greenmedinfo--2020-12-17--Hydroxysafflor yellow A ameliorates homocysteine-induced Alzheimer-like pathologic dysfunction and m

Hydroxysafflor yellow A ameliorates homocysteine-induced Alzheimer-like pathologic dysfunction and memory/synaptic disorder.

Homocysteine ( Hcy ) could induce amyloidβ ( Aβ ) accumulation , synaptic dysfunction , and memory impairment as seen @ @ @ @ @ ) , the most prevalent neurodegenerative disorder , which affects more than 25 million people @ @ @ @ @ the protective effect of hydroxysafflor yellow A ( HSYA ) on Hcy-induced Aβ accumulation , @ @ @ @ @ and memory deficits .
Rats were randomly divided into four groups : Control group , @ @ @ @ @ NS ) ; Hcy group , which received a daily vena caudalis injection of Hcy @ @ @ @ @ ) ; Hcy+HSYA group , which received the same amount ofHcy plus 6 mg/kg per @ @ @ @ @ HSYA group , which received 6 mg/kg per day HSYA intraperitoneally for 2 weeks .
@ @ @ @ @ of HSYA significantly attenuated Aβ accumulation , improved synaptic function , and reversed Hcy-induced cognitive @ @ @ @ @ that HSYA might be a promising therapeutic candidate for attenuating Hcy-induced AD-like pathological and behavioral @ @

Homocysteine (Hcy) could induce amyloidβ (Aβ) accumulation, synaptic dysfunction, and memory impairment as seen in Alzheimer disease (AD), the most prevalent neurodegenerative disorder, which affects more than 25 million people worldwide. Here we investigated the protective effect of hydroxysafflor yellow A (HSYA) on Hcy-induced Aβ accumulation, synaptic dysfunction, and learning and memory deficits. Rats were randomly divided into four groups: Control group, which received normal saline (NS); Hcy group, which received a daily vena caudalis injection of Hcy (400 μg/kg per day); Hcy+HSYA group, which received the same amount ofHcy plus 6 mg/kg per day HSYA intraperitoneally; and HSYA group, which received 6 mg/kg per day HSYA intraperitoneally for 2 weeks. Results showed that simultaneous supplementation of HSYA significantly attenuated Aβ accumulation, improved synaptic function, and reversed Hcy-induced cognitive impairment. Our data suggest that HSYA might be a promising therapeutic candidate for attenuating Hcy-induced AD-like pathological and behavioral deficits.


greenmedinfo--2020-12-17--Protective effects of hydroxysafflor yellow A on alcohol-induced liver injury.

Hydroxysafflor yellow A ( HSYA ) , the main active natural constituent extracted from Carthamus tinctorius L. , has been widely used for the treatment of cerebrovascular and cardiovascular diseases .
The aim of this study is to explore the effect of HSYA on alcohol-induced liver injury and the underlying mechanism .
Male Sprague-Dawley rats were used to establish the liver injury model induced by alcohol .
HSYA treatment ameliorated serum biochemical indicators by reducing the levels of alanine aminotransferase ( ALT ) , aspartate aminotransferase ( AST ) , hyaluronan ( HA ) , laminin ( LN ) , @ @ @ @ @ @ @ in rats .
HSYA efficiently increased the activity and messenger RNA ( mRNA ) of superoxide dismutase ( SOD ) and glutathione peroxidase ( GPx ) in rat liver tissue compared with those of model group , which was obviously reduced by alcohol .
HSYA also apparently decreased the levels of reactive oxygen species ( ROS ) and malondialdehyde ( MDA ) in rat liver tissue compared with those of model group , which was obviously enhanced by alcohol .
Histological studies demonstrated that HSYA substantially reduced the number of macro- and micro-vesicular @ @ @ @ @ @ @ ballooning degeneration areas , ameliorated the severity of liver damage induced by long-term drinking , and finally improved the liver architecture .
In addition , immunohistochemistry study indicated that the activation of transforming growth factorβ1 ( TGF-β1 ) stimulated by alcohol in rat liver tissue was significantly blocked by HSYA .
Collectively , these data demonstrated that HSYA can effectively protect the liver of rats from long-term alcohol injury , which relates with the enhanced antioxidant capacity of liver tissues and inhibition ofTGF-β1 expression .

Hydroxysafflor yellow A (HSYA), the main active natural constituent extracted from Carthamus tinctorius L., has been widely used for the treatment of cerebrovascular and cardiovascular diseases. The aim of this study is to explore the effect of HSYA on alcohol-induced liver injury and the underlying mechanism. Male Sprague-Dawley rats were used to establish the liver injury model induced by alcohol. HSYA treatment ameliorated serum biochemical indicators by reducing the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronan (HA), laminin (LN), and type III precollagen (III-C) in rats. HSYA efficiently increased the activity and messenger RNA (mRNA) of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in rat liver tissue compared with those of model group, which was obviously reduced by alcohol. HSYA also apparently decreased the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) in rat liver tissue compared with those of model group, which was obviously enhanced by alcohol. Histological studies demonstrated that HSYA substantially reduced the number of macro- and micro-vesicular steatosis, suppressed hepatic fibrogenesis and shrunk ballooning degeneration areas, ameliorated the severity of liver damage induced by long-term drinking, and finally improved the liver architecture. In addition, immunohistochemistry study indicated that the activation of transforming growth factorβ1 (TGF-β1) stimulated by alcohol in rat liver tissue was significantly blocked by HSYA. Collectively, these data demonstrated that HSYA can effectively protect the liver of rats from long-term alcohol injury, which relates with the enhanced antioxidant capacity of liver tissues and inhibition ofTGF-β1 expression.


greenmedinfo--2020-12-17--Hydroxysafflor yellow A inhibits angiogenesis of hepatocellular carcinoma.

Hydroxysafflor yellow A ( HSYA ) , a flavonoid derived and isolated from traditional Chinese medicine Carthamus tinctorius L. , possesses anti-tumor activity .
However , its effects on hepatocellular carcinoma ( HCC ) have not been investigated .
The proliferation and metastasis of HCC are dependent on angiogenesis , which also strongly links with several signal transduction pathways associated with cell proliferation and apoptosis .
This study aimed to explore the effect of HSYA on vasculogenesis and to determine its molecular mechanism by investigating the expression of ERK/MAPK ( p-c-Raf , c-Raf , p-ERK1/2 , ERK1/2 ) and NF-κB @ @ @ @ @ @ @ signaling pathway in H22 tumor-bearing mice .
The results showed that HSYA could considerably suppress tumor growth by inhibiting secretion of angiogenesis factors ( vascular endothelial growth factor A , basic fibroblast growth factor ) and vascular endothelial growth factorreceptor1 .
At the moleculcould block ERK1/2 phosphorylation and then restrain the activation of NF-κB and its nuclear translocation by down-regulating the expression of p65 in the nucleus , up-regulating p65 level in the cytoplasm , inhibiting IκB phosphorylation and cytoplasmic degradation of IκB-α .
Finally , we demonstrate that HSYA could suppress mRNA @ @ @ @ @ @ @ cyclinD1 , c-myc , c-Fos ) compared with negative control group .
And best of all , HSYA could improve spleen/thymus indexes , which was evaluated as the marker of protective effect on the immune system .
Our findings support HSYA as a promising candidate for the prevention and treatment of HCC .

Hydroxysafflor yellow A (HSYA), a flavonoid derived and isolated from traditional Chinese medicine Carthamus tinctorius L., possesses anti-tumor activity. However, its effects on hepatocellular carcinoma (HCC) have not been investigated. The proliferation and metastasis of HCC are dependent on angiogenesis, which also strongly links with several signal transduction pathways associated with cell proliferation and apoptosis. This study aimed to explore the effect of HSYA on vasculogenesis and to determine its molecular mechanism by investigating the expression of ERK/MAPK (p-c-Raf, c-Raf, p-ERK1/2, ERK1/2) and NF-κB (p65, IκB and p-IκB) signaling pathway in H22 tumor-bearing mice. The results showed that HSYA could considerably suppress tumor growth by inhibiting secretion of angiogenesis factors (vascular endothelial growth factor A, basic fibroblast growth factor) and vascular endothelial growth factorreceptor1. At the moleculcould block ERK1/2 phosphorylation and then restrain the activation of NF-κB and its nuclear translocation by down-regulating the expression of p65 in the nucleus, up-regulating p65 level in the cytoplasm, inhibiting IκB phosphorylation and cytoplasmic degradation of IκB-α. Finally, we demonstrate that HSYA could suppress mRNA expression levels of cell proliferation-related genes (cyclinD1, c-myc, c-Fos) compared with negative control group. And best of all, HSYA could improve spleen/thymus indexes, which was evaluated as the marker of protective effect on the immune system. Our findings support HSYA as a promising candidate for the prevention and treatment of HCC.


greenmedinfo--2020-12-17--Hydroxysafflor yellow A exerts neuroprotective effects in cerebral ischemia reperfusion.

The innate immune response , which is tightly regulated by Toll-like receptor 4 ( TLR4 ) pathway , has been shown to play a critical role in brain damage following cerebral ischemia-reperfusion injury .
Hydroxysafflor yellow A ( HSYA ) is the active component extracted from the Flos Carthami and has been reported to decrease neurological deficit scores following ischemia-reperfusion injury .
However , the precise mechanism by which it exerts these neuroprotective effects remains poorly understood .
In this study , we demonstrated that the administration of HSYA could significantly down-regulate TLR4 expression in middle cerebral artery occlusion ( @ @ @ @ @ @ @ of TLR4 by HSYA treatment , cerebral infarction and inflammatory neuronal damage was alleviated .
The number of apoptotic neurons in the HSYA-treated group was significantly decreased along with the decrease in TLR4 expression in MCAO mice .
Activation of the NF-κB and MAPK signaling pathways was observed at 1h following ischemia and at 24h post-reperfusion .
HSYA could significantly inhibit NF-κB p-p65 , ERE1/2 , JNK and p38 phosphorylation , which coincided with the suppressed secretion of inflammatory cytokines such as tumor necrosis factor-α ( TNF-α ) , interleukin-1β ( IL-1β ) @ @ @ @ @ @ @ Moreover , brain-derived neurotrophic factor ( BDNF ) was up-regulated following 1h of ischemia and continued to increase initially during reperfusion but was down-regulated at later stages .
Following treatment with HSYA , BDNF was up-regulated relative to control MCAO mice at 1h post-ischemia and at 12 and 24h post-reperfusion .
Our data suggest that HSYA exerts neurotrophic and anti-inflammatory functions against ischemic stroke by inhibiting TLR4 pathway-mediated signaling responses .

The innate immune response, which is tightly regulated by Toll-like receptor 4 (TLR4) pathway, has been shown to play a critical role in brain damage following cerebral ischemia-reperfusion injury. Hydroxysafflor yellow A (HSYA) is the active component extracted from the Flos Carthami and has been reported to decrease neurological deficit scores following ischemia-reperfusion injury. However, the precise mechanism by which it exerts these neuroprotective effects remains poorly understood. In this study, we demonstrated that the administration of HSYA could significantly down-regulate TLR4 expression in middle cerebral artery occlusion (MCAO) mice. Following the down-regulation of TLR4 by HSYA treatment, cerebral infarction and inflammatory neuronal damage was alleviated. The number of apoptotic neurons in the HSYA-treated group was significantly decreased along with the decrease in TLR4 expression in MCAO mice. Activation of the NF-κB and MAPK signaling pathways was observed at 1h following ischemia and at 24h post-reperfusion. HSYA could significantly inhibit NF-κB p-p65, ERE1/2, JNK and p38 phosphorylation, which coincided with the suppressed secretion of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and nitric oxide (NO). Moreover, brain-derived neurotrophic factor (BDNF) was up-regulated following 1h of ischemia and continued to increase initially during reperfusion but was down-regulated at later stages. Following treatment with HSYA, BDNF was up-regulated relative to control MCAO mice at 1h post-ischemia and at 12 and 24h post-reperfusion. Our data suggest that HSYA exerts neurotrophic and anti-inflammatory functions against ischemic stroke by inhibiting TLR4 pathway-mediated signaling responses.


greenmedinfo--2020-12-17--Hydroxysafflor yellow A attenuates bleomycin-induced pulmonary fibrosis.

Hydroxysafflor yellow A ( HSYA ) is an active component of Carthamus tinctorius L. , and we want to investigate whether HSYA attenuates pulmonary fibrosis induced by bleomycin ( BLM ) in mice .
The mice received a BLM via oropharyngeal aspiration , and HSYA was intraperitoneally injected .
Arterial blood gas analysis was performed .
Morphological changes and hydroxyproline content were measured .
mRNA expression of transforming growth factor-β1 ( TGF-β1 ) , connective tissue growth factor , α-smooth muscle actin ( α-SMA ) , and collagen I was measured by real-time polymerase chain reaction .
α-SMA-positive cells in @ @ @ @ @ @ @ .
A549 cell was cultured , and morphological changes were observed after TGF-β1 and HSYA treatment .
mRNA expression was detected by real-time polymerase chain reaction .
Phosphorylation of Smad3 was evaluated by western blotting .
HSYA decreased the lung consolidation area and collagen deposition in mice with pulmonary fibrosis .
The blood gas changes due to BLM were attenuated by HSYA .
HSYA also alleviated the BLM-induced increase of TGF-β1 , connective tissue growth factor , α-SMA , and collagen I mRNA levels .
HSYA treatment inhibited the increase of α-SMA expression @ @ @ @ @ @ @ in lung tissue .
HSYA inhibits Smad3 phosphorylation and elevated expression of collagen I mRNA in epithelial-mesenchymal transition induced by TGF-β1 .

Hydroxysafflor yellow A (HSYA) is an active component of Carthamus tinctorius L., and we want to investigate whether HSYA attenuates pulmonary fibrosis induced by bleomycin (BLM) in mice. The mice received a BLM via oropharyngeal aspiration, and HSYA was intraperitoneally injected. Arterial blood gas analysis was performed. Morphological changes and hydroxyproline content were measured. mRNA expression of transforming growth factor-β1 (TGF-β1), connective tissue growth factor, α-smooth muscle actin (α-SMA), and collagen I was measured by real-time polymerase chain reaction. α-SMA-positive cells in lung tissues were detected by immunohistochemical staining. A549 cell was cultured, and morphological changes were observed after TGF-β1 and HSYA treatment. mRNA expression was detected by real-time polymerase chain reaction. Phosphorylation of Smad3 was evaluated by western blotting. HSYA decreased the lung consolidation area and collagen deposition in mice with pulmonary fibrosis. The blood gas changes due to BLM were attenuated by HSYA. HSYA also alleviated the BLM-induced increase of TGF-β1, connective tissue growth factor, α-SMA, and collagen I mRNA levels. HSYA treatment inhibited the increase of α-SMA expression, Smad3 phosphorylation, the morphological changes in lung tissue. HSYA inhibits Smad3 phosphorylation and elevated expression of collagen I mRNA in epithelial-mesenchymal transition induced by TGF-β1.


greenmedinfo--2020-12-17--Hydroxysafflor yellow A increases BDNF and NMDARs in the hippocampus in a vascular dementia.

Hydroxysafflor yellow A ( HSYA ) is a drug that exerts angiogenesis regulatory and neuroprotective effects and has become an effective therapy for brain and heart ischemic disorders .
There is no definite evidence supporting a therapeutic effect of HSYA in vascular dementia ( VaD ) .
We used HSYA in a rat model of chronic cerebral ischemia to determine its potential therapeutic effects in VaD .
The Morris water maze ( MWM ) was used to evaluate spatial cognitive function , and long-term potentiation ( LTP ) was tested as a marker of synaptic plasticity .
The expression levels @ @ @ @ @ @ @ and two subunits of N-methyl-d-aspartate receptor ( NMDAR ; GluN2A and GluN2B ) in the hippocampus were measured via western blotting .
The MWM results showed that the experimental VaD group had longer escape latencies than the sham group , whereas the HSYA group had a decreased escape latency compared with the VaD group ( P < 0.05 ) .
The LTP at CA3-CA1 synapses in the hippocampus was also enhanced in the HSYA compared with the VaD group ( P < 0.05 ) .
The western blotting results revealed lower hippocampal BDNF @ @ @ @ @ @ @ compared with the sham group and significantly higher hippocampal expression in the HSYA group compared with the VaD group .
No significant change in GluN2A expression was detected .
The results indicate that HSYA may enhance the endogenous expression of BDNF and GluN2B , which are associated with the synaptic plasticity of the hippocampus , and may improve spatial learning and memory abilities in a rat model of VaD .

Hydroxysafflor yellow A (HSYA) is a drug that exerts angiogenesis regulatory and neuroprotective effects and has become an effective therapy for brain and heart ischemic disorders. There is no definite evidence supporting a therapeutic effect of HSYA in vascular dementia (VaD). We used HSYA in a rat model of chronic cerebral ischemia to determine its potential therapeutic effects in VaD. The Morris water maze (MWM) was used to evaluate spatial cognitive function, and long-term potentiation (LTP) was tested as a marker of synaptic plasticity. The expression levels of brain-derived neurotrophic factor (BDNF) and two subunits of N-methyl-d-aspartate receptor (NMDAR; GluN2A and GluN2B) in the hippocampus were measured via western blotting. The MWM results showed that the experimental VaD group had longer escape latencies than the sham group, whereas the HSYA group had a decreased escape latency compared with the VaD group (P<0.05). The LTP at CA3-CA1 synapses in the hippocampus was also enhanced in the HSYA compared with the VaD group (P<0.05). The western blotting results revealed lower hippocampal BDNF and GluN2B expression in the VaD group compared with the sham group and significantly higher hippocampal expression in the HSYA group compared with the VaD group. No significant change in GluN2A expression was detected. The results indicate that HSYA may enhance the endogenous expression of BDNF and GluN2B, which are associated with the synaptic plasticity of the hippocampus, and may improve spatial learning and memory abilities in a rat model of VaD.


greenmedinfo--2020-12-17--Hydroxysafflor yellow A had a protective effect against fibrosis in renal cells.

OBJECTIVE : Renal fibrosis is the common pathological foundation of many chronic kidney diseases ( CKDs ) .
The aim of this study was to investigate whether Hydroxysafflor yellow A ( HSYA ) can preserve renal function by inhibiting the progression of renal fibrosis and the potential mechanisms .
METHODS : Renal fibrosis was induced by unilateral ureteral obstruction ( UUO ) performed on 7-week-old C57BL/6 mice .
HSYA ( 10 , 50 and 100 mg/kg ) were intragastrically administered .
Sham group and model group were administered with the same volume of vehicle .
Serum and kidney samples were @ @ @ @ @ @ @ .
Serum biochemical indicators were measured by automatic biochemical analyzer .
Histological changes were evaluated by HE and Masson staining .
In vitro , the anti-fibrotic effect of HSYA was tested on human recombinant transforming growth factor-β1 ( TGF-β1 ) stimulated HK-2 cells .
The protein levels of α-SMA , collagen-I and fibronectin in kidney tissue and HK-2 cells were measured by immunohistochemistry and immunofluorescence .
The protein levels of apoptosis-relative and TGF-β1/Smad3 signaling were detected by western blot .
RESULTS : HSYA slowed the development of renal fibrosis both in vivo and @ @ @ @ @ @ @ renal function index suggested that HSYA treatment decreased the level of serum creatinine ( Scr ) and blood urea nitrogen ( BUN ) rose by UUO ( P < 0.05 ) .
HE staining and Masson staining demonstrated that kidney interstitial fibrosis , tubular atrophy , and inflammatory cell infiltration were notably attenuated in the high-dose HSYA group compared with the model group .
The expressions ofα-SMA , collagen-I and fibronectin were decreased in the UUO kidney and HK-2 cells of the HSYA-treatment group .
Moreover , HSYA reduced the apoptotic rate of @ @ @ @ @ @ @ study revealed that HSYA regulated the TGF-β1/Smads signaling pathway both in kidney tissue and HK-2cells .
CONCLUSIONS : These results suggested that HSYA had a protective effect against fibrosis in renal cells , at least partly , through inhibiting TGF-β1/smad3-mediated Epithelial-mesenchymal transition signaling pathway .

OBJECTIVE: Renal fibrosis is the common pathological foundation of many chronic kidney diseases (CKDs). The aim of this study was to investigate whether Hydroxysafflor yellow A (HSYA) can preserve renal function by inhibiting the progression of renal fibrosis and the potential mechanisms.
METHODS: Renal fibrosis was induced by unilateral ureteral obstruction (UUO) performed on 7-week-old C57BL/6 mice. HSYA (10, 50 and 100 mg/kg) were intragastrically administered. Sham group and model group were administered with the same volume of vehicle. Serum and kidney samples were collected 14 days after the UUO surgery. Serum biochemical indicators were measured by automatic biochemical analyzer. Histological changes were evaluated by HE and Masson staining. In vitro, the anti-fibrotic effect of HSYA was tested on human recombinant transforming growth factor-β1 (TGF-β1) stimulated HK-2 cells. The protein levels of α-SMA, collagen-I and fibronectin in kidney tissue and HK-2 cells were measured by immunohistochemistry and immunofluorescence. The protein levels of apoptosis-relative and TGF-β1/Smad3 signaling were detected by western blot.
RESULTS: HSYA slowed the development of renal fibrosis both in vivo and in vitro. In UUO rats, renal function index suggested that HSYA treatment decreased the level of serum creatinine (Scr) and blood urea nitrogen (BUN) rose by UUO (P<0.05). HE staining and Masson staining demonstrated that kidney interstitial fibrosis, tubular atrophy, and inflammatory cell infiltration were notably attenuated in the high-dose HSYA group compared with the model group. The expressions ofα-SMA, collagen-I and fibronectin were decreased in the UUO kidney and HK-2 cells of the HSYA-treatment group. Moreover, HSYA reduced the apoptotic rate of HK-2 cells stimulated by TGF-β1. Further study revealed that HSYA regulated the TGF-β1/Smads signaling pathway both in kidney tissue and HK-2cells.
CONCLUSIONS: These results suggested that HSYA had a protective effect against fibrosis in renal cells, at least partly, through inhibiting TGF-β1/smad3-mediated Epithelial-mesenchymal transition signaling pathway.


greenmedinfo--2020-12-17--A review of the effect of Boswellia species on metabolic syndrome.

The metabolic syndrome , a cluster of metabolic disorders , includes abdominal obesity , hypertension , dyslipidemia , and hyperglycemia leading to insulin resistance , development of diabetes mellitus , and cardiovascular diseases .
For the treatment of metabolic syndrome , traditional herbal medicines such as frankincense orspecies have been used due to their anti-inflammatory , anti-oxidant , anti-obesity , antidiabetic , antihypertensive , and hypolipidemic properties .
Based on the literature , published evidence up to 2020 about the therapeutic effects ofspecies on the metabolic disorder among Medline , Scopus , and Google Scholar were precisely evaluated by keywords @ @ @ @ @ @ @ , hypertension , blood pressure , dyslipidemia , metabolic syndrome , frankincense , and Boswellia .
According to the results , species have beneficial effects to control metabolic syndrome and its related disorders such as hyperglycemia , dyslipidemia , hypertension , obesity , diabetes , and its complications.species by reducing the resistance to insulin and restoring pancreatic beta cells decrease blood glucose .
Also , species has antithrombotic and anticoagulant properties that regulate blood pressure .
The anti-oxidant properties ofspecies modulate the blood lipid profile via reducing TNF-α , IL-1β levels , and @ @ @ @ @ @ @ and protective effects ofspecies on metabolic disorders were remarkably confirmed regarding decreasing hyperglycemia , hyperlipidemia , hypertension , and obesity .

The metabolic syndrome, a cluster of metabolic disorders, includes abdominal obesity, hypertension, dyslipidemia, and hyperglycemia leading to insulin resistance, development of diabetes mellitus, and cardiovascular diseases. For the treatment of metabolic syndrome, traditional herbal medicines such as frankincense orspecies have been used due to their anti-inflammatory, anti-oxidant, anti-obesity, antidiabetic, antihypertensive, and hypolipidemic properties. Based on the literature, published evidence up to 2020 about the therapeutic effects ofspecies on the metabolic disorder among Medline, Scopus, and Google Scholar were precisely evaluated by keywords such as obesity, diabetes, hyperglycemia, hypertension, blood pressure, dyslipidemia, metabolic syndrome, frankincense, and Boswellia. According to the results,species have beneficial effects to control metabolic syndrome and its related disorders such as hyperglycemia, dyslipidemia, hypertension, obesity, diabetes, and its complications.species by reducing the resistance to insulin and restoring pancreatic beta cells decrease blood glucose. Also,species has antithrombotic and anticoagulant properties that regulate blood pressure. The anti-oxidant properties ofspecies modulate the blood lipid profile via reducing TNF-α, IL-1β levels, and increasing the adiponectin level. The therapeutic and protective effects ofspecies on metabolic disorders were remarkably confirmed regarding decreasing hyperglycemia, hyperlipidemia, hypertension, and obesity.


greenmedinfo--2020-12-17--Curcuminoids and boswellia serrata extracts combination decreases tendinopathy symptoms.

To investigate the effects of one-month treatment in addition to standard care with a food supplement containing both Curcuma longa @ @ @ @ @ tendinopathy symptoms..
This open-label , non-controlled , post-observational study included 670 patients suffering from tendinopathy @ @ @ @ @ Belgian general practitioners .
Patients received a medical prescription for one-month treatment with two tablets @ @ @ @ @ pharmaceutical grade food supplement containing both Curcuma Longa and Boswellia serrata extracts .
Pain and @ @ @ @ @ a visual analog scale at the inclusion and one-month treatment later .
Patient satisfaction , @ @ @ @ @ effects were also recorded.. After one-month treatment , pain and functional limitation were significantly improved @ @ @ @ @ , its localization , and the duration of symptoms .
The pain score decreased from @ @ @ @ @ ± 1.64 ( p

To investigate the effects of one-month treatment in addition to standard care with a food supplement containing both Curcuma longa and Boswellia serrata extracts on tendinopathy symptoms.. This open-label, non-controlled, post-observational study included 670 patients suffering from tendinopathy recruited at different sites by Belgian general practitioners. Patients received a medical prescription for one-month treatment with two tablets twice a day of a pharmaceutical grade food supplement containing both Curcuma Longa and Boswellia serrata extracts. Pain and functional limitation were evaluated using a visual analog scale at the inclusion and one-month treatment later. Patient satisfaction, concomitant drugs intake and side effects were also recorded.. After one-month treatment, pain and functional limitation were significantly improved whatever the cause of tendinopathy, its localization, and the duration of symptoms. The pain score decreased from 6.16 ± 1.53 to 2.98 ± 1.64 (p < 0.0001), yielding a drop of 51.6% and the functional limitation score fell after one-month treatment from 5.96 ± 1.73 to 2.88 ± 1.67 (p<0.0001) corresponding to a drop of 51.6%. The percentage of patients taking at least one concomitant treatment at the end of the treatment period had decreased from 81.3% to 61.8% (p < 0.0001). Only 43 (6.5%) patients reported side effects. No severe adverse effects related to the product were reported.. The combination of Curcuma Longa and Boswellia serrata extracts improves symptoms in patients suffering of tendinopathy and shows a good safety. Although its effect will have to be confirmed in randomized controlled trials, it can be considered as a helpful support of standard symptomatic treatments for tendinopathies. Highlights: Tendinopathy is a common disease representing 30% of all consultations with a general practitioner for musculoskeletal disorders. The combination of Curcuminoids and Boswellia serrata extracts are efficient on tendinopathy symptoms in support of standard symptomatic treatments. The combination of Curcuminoids and Boswellia Serrata extract is safe and can be administrated for at least one month in addition of analgesic and non-steroidal anti-inflammatory drugs.


greenmedinfo--2020-12-17--Antioxidant effects of hydroxysafflor yellow A and acetyl-11-keto-β-boswellic acid in combination on

Antioxidant effects of hydroxysafflor yellow A and acetyl-11-keto-β-boswellic acid in combination on isoproterenol-induced myocardial injury.

Oxidative stress plays an important role in the initiation and development of myocardial injury ( MI ) .
The peroxisome proliferator-activated receptor gamma coactivator-1α ( PGC‑1α ) /nuclear factor erythroid 2-related factor 2 ( Nrf2 ) pathway is considered to be a potential target for cardioprotection in MI .
Acetyl-11-keto-β-boswellic acid ( AKBA ) is the major organic acid component extracted from Boswellia serrata Roxb .
ex Colebr .
Hydroxysafﬂor yellow A ( HSYA ) is the principal active constituent of Carthamus tinctorius L. In the present study , we aimed to investigate the cardioprotective effects of HSYA and AKBA @ @ @ @ @ @ @ , as well as the underlying mechanisms responsible for these effects .
For this purpose , MI was produced in Sprague-Dawley rats by subcutaneous injection with isoproterenol .
To model ischemic-like conditions in vitro , H9C2 cells were subjected to oxygen-glucose deprivation ( OGD ) .
The levels of creatine kinase-MB ( CK‑MB ) , lactate dehydrogenase ( LDH ) , malondialdehyde ( MDA ) as well as superoxide dismutase ( SOD ) activity were examined as well as apoptotic cell death .
Mitochondrial reactive oxygen species ( ROS ) production and mitochondrial @ @ @ @ @ @ @ were measured using MitoSOX Red and 5,5',6,6'-tetraethylbenzimidazolylcarbocyanine iodide ( JC-1 ) dye .
The expression of PGC-1α and Nrf2 was quantified by western blot analysis and immunohistochemistry .
HSYA and AKBA prevented myocardial pathological changes , signiﬁcantly reduced the blood levels of CK-MB and LDH , and decreased apoptotic cell death .
They significantly increased the expression of PGC-1α and Nrf2 , and the activity of the antioxidant enzyme SOD and also decreased the levels of MDA and ROS .
Moreover , the reduction in MMP was partly prevented by HSYA and AKBA @ @ @ @ @ @ @ the underlyingmechanisms through which HSYA and AKBA protect against MI .
Additionally , HSYA and AKBA appear to act synergistically in order to exert cardioprotective effects .

Oxidative stress plays an important role in the initiation and development of myocardial injury (MI). The peroxisome proliferator-activated receptor gamma coactivator-1α (PGC‑1α)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway is considered to be a potential target for cardioprotection in MI. Acetyl-11-keto-β-boswellic acid (AKBA) is the major organic acid component extracted from Boswellia serrata Roxb. ex Colebr. Hydroxysafﬂor yellow A (HSYA) is the principal active constituent of Carthamus tinctorius L. In the present study, we aimed to investigate the cardioprotective effects of HSYA and AKBA in combination in vivo and in vitro, as well as the underlying mechanisms responsible for these effects. For this purpose, MI was produced in Sprague-Dawley rats by subcutaneous injection with isoproterenol. To model ischemic-like conditions in vitro, H9C2 cells were subjected to oxygen-glucose deprivation (OGD). The levels of creatine kinase-MB (CK‑MB), lactate dehydrogenase (LDH), malondialdehyde (MDA) as well as superoxide dismutase (SOD) activity were examined as well as apoptotic cell death. Mitochondrial reactive oxygen species (ROS) production and mitochondrial membrane potential (ΔΨm or MMP) were measured using MitoSOX Red and 5,5',6,6'-tetraethylbenzimidazolylcarbocyanine iodide (JC-1) dye. The expression of PGC-1α and Nrf2 was quantified by western blot analysis and immunohistochemistry. HSYA and AKBA prevented myocardial pathological changes, signiﬁcantly reduced the blood levels of CK-MB and LDH, and decreased apoptotic cell death. They significantly increased the expression of PGC-1α and Nrf2, and the activity of the antioxidant enzyme SOD and also decreased the levels of MDA and ROS. Moreover, the reduction in MMP was partly prevented by HSYA and AKBA. Taken together, these findings elucidate the underlyingmechanisms through which HSYA and AKBA protect against MI. Additionally, HSYA and AKBA appear to act synergistically in order to exert cardioprotective effects.


greenmedinfo--2020-12-17--Hydroxysafﬂor yellow A exerts antioxidant effects in a rat model of traumatic brain injury.

Free radical-induced oxidative damage occurs rapidly and is of primary importance during the secondary pathophysiological cascades of traumatic brain injury ( TBI ) .
Hydroxysafflor yellow A ( HSYA ) is a constituent of the flower petals of Carthamus tinctorius ( safflower ) and may represent a potential therapeutic strategy to improve outcomes following TBI .
The present study aimed to identify HSYA in the brain tissues of rats exposed to TBI to determine its absorption and to investigate the underlying effects of HSYA on antioxidant enzymes in the brain tissues of TBI rats .
To determine the absorption of @ @ @ @ @ @ @ antioxidant effects of HSYA in TBI , the presence of HSYA in the brain tissues of the TBI rats was identified using an ultra performance liquid chromatography‑tandem mass spectrometry method .
Subsequently , the state of oxidative stress in the TBI rat model following the administration of HSYA was investigated by determining the levels of antioxidant enzymes , including superoxide dismutase ( SOD ) , malondialdehyde ( MDA ) and catalase ( CAT ) , and the ratio of glutathione ( GSH ) /glutathione disulfide ( GSSG ) .
The data obtained demonstrated @ @ @ @ @ @ @ tissues of the TBI rats .
HSYA increased the activities of SOD and CAT , the level of GSH and the GSH/GSSG ratio .
However , HSYA concomitantly decreased the levels of MDA and GSSG .
Thesepreliminary data suggest that HSYA has the potential to be utilized as a neuroprotective drug in cases of TBI .

Free radical-induced oxidative damage occurs rapidly and is of primary importance during the secondary pathophysiological cascades of traumatic brain injury (TBI). Hydroxysafflor yellow A (HSYA) is a constituent of the flower petals of Carthamus tinctorius (safflower) and may represent a potential therapeutic strategy to improve outcomes following TBI. The present study aimed to identify HSYA in the brain tissues of rats exposed to TBI to determine its absorption and to investigate the underlying effects of HSYA on antioxidant enzymes in the brain tissues of TBI rats. To determine the absorption of HSYA for the investigation of the underlying antioxidant effects of HSYA in TBI, the presence of HSYA in the brain tissues of the TBI rats was identified using an ultra performance liquid chromatography‑tandem mass spectrometry method. Subsequently, the state of oxidative stress in the TBI rat model following the administration of HSYA was investigated by determining the levels of antioxidant enzymes, including superoxide dismutase (SOD), malondialdehyde (MDA) and catalase (CAT), and the ratio of glutathione (GSH)/glutathione disulfide (GSSG). The data obtained demonstrated that HSYA was absorbed in the brain tissues of the TBI rats. HSYA increased the activities of SOD and CAT, the level of GSH and the GSH/GSSG ratio. However, HSYA concomitantly decreased the levels of MDA and GSSG. Thesepreliminary data suggest that HSYA has the potential to be utilized as a neuroprotective drug in cases of TBI.


greenmedinfo--2020-12-17--Hydroxysafflor yellow A alleviates myocardial ischemia/reperfusion in hyperlipidemia.

Hyperlipidemia aggravates myocardial ischemia/reperfusion ( MI/R ) injury through stimulating excessive inflammatory response .
Therefore , blockade of inflammatory signal is a potential therapeutic management for MI/R complicated with hyperlipidemia .
Hydroxysafflor yellow A ( HSYA , a monomer extracted from Carthamus tinctorius L. ) , was studied in this article to address that the regulation of inflammatory signal would alleviate MI/R combined with hyperlipidemia injury .
High-fat diet induced hyperlipidemia worsened MI/R mediated heart injury ( elevation of infarct size , CK-MB and LDH activity ) , activated TLR4 over-expression in hearts , released inflammatory cytokines ( LPS , @ @ @ @ @ @ @ administration suppressed the over-expression of TLR4 and alleviated heart damage caused by MI/R complicated with hyperlipidemia .
Furthermore , HSYA had little influence on MI/R injury in TLR4-knockout mice , which indicated that HSYA protected MI/R through TLR4 inhibition .
In vitro , hypoxia/reoxygenation ( H/R ) coexisting with LPS model in neonatal rat ventricular myocytes ( NRVMs ) induced serious damage compared with H/R injury to NRVMs .
HSYA decreased excessive secretion of inflammatory cytokines , down-regulated over-expression of TLR4 and NF-κB in H/R + LPS injured NRVMs .
In conclusion , @ @ @ @ @ @ @ TLR4 , offering an alternative medication for MI/R associated with hyperlipidemia .

Hyperlipidemia aggravates myocardial ischemia/reperfusion (MI/R) injury through stimulating excessive inflammatory response. Therefore, blockade of inflammatory signal is a potential therapeutic management for MI/R complicated with hyperlipidemia. Hydroxysafflor yellow A (HSYA, a monomer extracted from Carthamus tinctorius L.), was studied in this article to address that the regulation of inflammatory signal would alleviate MI/R combined with hyperlipidemia injury. High-fat diet induced hyperlipidemia worsened MI/R mediated heart injury (elevation of infarct size, CK-MB and LDH activity), activated TLR4 over-expression in hearts, released inflammatory cytokines (LPS, TNF-α and IL-1β) excessively. HSYA administration suppressed the over-expression of TLR4 and alleviated heart damage caused by MI/R complicated with hyperlipidemia. Furthermore, HSYA had little influence on MI/R injury in TLR4-knockout mice, which indicated that HSYA protected MI/R through TLR4 inhibition. In vitro, hypoxia/reoxygenation (H/R) coexisting with LPS model in neonatal rat ventricular myocytes (NRVMs) induced serious damage compared with H/R injury to NRVMs. HSYA decreased excessive secretion of inflammatory cytokines, down-regulated over-expression of TLR4 and NF-κB in H/R + LPS injured NRVMs. In conclusion, HSYA alleviated myocardial inflammatory injury through suppressing TLR4, offering an alternative medication for MI/R associated with hyperlipidemia.


greenmedinfo--2020-12-17--These results indicate the potential utility of hydroxysafflor yellow A for the treatment of ischemi

These results indicate the potential utility of hydroxysafflor yellow A for the treatment of ischemic diseases.

BACKGROUND : The flowers of Carthamus tinctorius L. are widely used in traditional Chinese medicine to treat cerebrovascular and cardiovascular diseases .
Hydroxysafflor yellow A ( HSYA ) , the main constituent of C. tinctorius L. flowers , is known for its multiple biological activities .
The present study investigated the effects of HSYA on angiogenesis in vitro and in a mouse hindlimb ischemia model .
METHODS : Using human umbilical vein endothelial cells ( HUVEC ) in vitro and a mouse hindlimb ischemia model in vivo , the angiogenic role of HSYA was evaluated .
RESULTS : HSYA significantly @ @ @ @ @ @ @ of HUVEC .
HSYA not only induced a rise in the expression of angiopoietin 1 and Tie-2 but it also increased phosphorylation of Tie-2 , Akt , and extracellular signal-regulated kinase 1/2 .
Furthermore , an anti-Tie-2 neutralizing antibody significantly inhibited HSYA-induced HUVEC tube formation and migration .
In vivo , the recovery of perfusion of ischemic hindlimb tissue after femoral artery interruption was significantly increased in HSYA-treated mice compared to vehicle controls .
Consistent with these results , the arteriole and capillary densities in ischemic gastrocnemius muscles were significantly increased in HSYA-treated @ @ @ @ @ @ @ the potential utility of HSYA for the treatment of ischemic diseases .

BACKGROUND: The flowers of Carthamus tinctorius L. are widely used in traditional Chinese medicine to treat cerebrovascular and cardiovascular diseases. Hydroxysafflor yellow A (HSYA), the main constituent of C. tinctorius L. flowers, is known for its multiple biological activities. The present study investigated the effects of HSYA on angiogenesis in vitro and in a mouse hindlimb ischemia model.
METHODS: Using human umbilical vein endothelial cells (HUVEC) in vitro and a mouse hindlimb ischemia model in vivo, the angiogenic role of HSYA was evaluated.
RESULTS: HSYA significantly increased the capillary-like tube formation and migration of HUVEC. HSYA not only induced a rise in the expression of angiopoietin 1 and Tie-2 but it also increased phosphorylation of Tie-2, Akt, and extracellular signal-regulated kinase 1/2. Furthermore, an anti-Tie-2 neutralizing antibody significantly inhibited HSYA-induced HUVEC tube formation and migration. In vivo, the recovery of perfusion of ischemic hindlimb tissue after femoral artery interruption was significantly increased in HSYA-treated mice compared to vehicle controls. Consistent with these results, the arteriole and capillary densities in ischemic gastrocnemius muscles were significantly increased in HSYA-treated mice.
CONCLUSIONS: These results indicate the potential utility of HSYA for the treatment of ischemic diseases.


greenmedinfo--2020-12-17--The results additionally demonstrated that hydroxysafflor yellow A could enhance superoxide dismutas

The results additionally demonstrated that hydroxysafflor yellow A could enhance superoxide dismutase.

Hepatic fibrosis is a reversible pathological process , in which fibrotic tissue is excessively deposited in the liver during the repair process that follows hepatic injury .
Early prevention or treatment of hepatic fibrosis has great significance on the treatment of chronic hepatic diseases .
Hydroxysafflor yellow A ( HSYA ) is a water-soluble monomer extracted from safflower , which serves numerous pharmacological roles .
However , it remains to be elucidated how HSYA regulates hepatic fibrogenesis .
The aim of the present study was to reveal the possible mechanisms underlying the effects of HSYA on the prevention and treatment @ @ @ @ @ @ @ of hepatic fibrosis was established in the present study , and the rats were administered various doses of HSYA .
The effects of HSYA on pathological alterations of the liver tissue in rats with hepatic fibrosis were observed using hematoxylin-eosin staining and Masson staining .
In order to explore the anti‑hepatic fibrosis effects and underlying mechanisms of HSYA , serum levels , and hepatic function and hepatic fibrosis indices were evaluated .
The results demonstrated that HSYA can improve the general condition of rats with hepatic fibrosis and relieve cellular swelling of the @ @ @ @ @ @ @ inflammatory cell infiltration and fibroplastic proliferation .
Subsequent to administration of HSYA , globulin was increased during hepatic fibrosis caused by tetrachloromethane .
However , total cholesterol , triglyceride , alanineaminotransferase , aspartate aminotransferase and levels of hyaluronic acid , laminin , procollagen Ⅲ N‑terminal peptide , collagen type Ⅳ and hydroxyproline were significantly reduced .
The results additionally demonstrated that HSYA could enhance superoxide dismutase activity and reduce malondialdehyde levels , inhibiting lipid peroxidation caused by free radicals .

Hepatic fibrosis is a reversible pathological process, in which fibrotic tissue is excessively deposited in the liver during the repair process that follows hepatic injury. Early prevention or treatment of hepatic fibrosis has great significance on the treatment of chronic hepatic diseases. Hydroxysafflor yellow A (HSYA) is a water-soluble monomer extracted from safflower, which serves numerous pharmacological roles. However, it remains to be elucidated how HSYA regulates hepatic fibrogenesis. The aim of the present study was to reveal the possible mechanisms underlying the effects of HSYA on the prevention and treatment of hepatic fibrosis. A rat model of hepatic fibrosis was established in the present study, and the rats were administered various doses of HSYA. The effects of HSYA on pathological alterations of the liver tissue in rats with hepatic fibrosis were observed using hematoxylin-eosin staining and Masson staining. In order to explore the anti‑hepatic fibrosis effects and underlying mechanisms of HSYA, serum levels, and hepatic function and hepatic fibrosis indices were evaluated. The results demonstrated that HSYA can improve the general condition of rats with hepatic fibrosis and relieve cellular swelling of the liver, fatty degeneration, necrosis, inflammatory cell infiltration and fibroplastic proliferation. Subsequent to administration of HSYA, globulin was increased during hepatic fibrosis caused by tetrachloromethane. However, total cholesterol, triglyceride, alanineaminotransferase, aspartate aminotransferase and levels of hyaluronic acid, laminin, procollagen Ⅲ N‑terminal peptide, collagen type Ⅳ and hydroxyproline were significantly reduced. The results additionally demonstrated that HSYA could enhance superoxide dismutase activity and reduce malondialdehyde levels, inhibiting lipid peroxidation caused by free radicals.


greenmedinfo--2020-12-17--Hydroxysafflor yellow A attenuates the expression of inflammatory cytokines in acute soft tissue inj

Hydroxysafflor yellow A attenuates the expression of inflammatory cytokines in acute soft tissue injury.

We examined the effect of hydroxysafflor yellow A ( HSYA ) on the inflammatory response to strike-induced acute soft tissue injury in rats .
Soft tissue injury was induced in rat leg muscles using a strike hammer , followed by intraperitoneal administration of HSYA at 16 , 32 , or 64 mg/kg .
After 24 h , the rats were anaesthetized , blood and muscle samples were taken .
Plasma levels of interleukin ( IL ) -6 , IL-1β , and tumour necrosis factor ( TNF ) -αwere measured by enzyme-linked immunosorbent assay .
Total RNA and protein were isolated @ @ @ @ @ @ @ levels of IL-6 , IL-1β , TNF-α , vascular cell adhesion molecule ( VCAM ) -1 , and intercellular adhesion molecule ( ICAM ) -1 , and the protein level of phosphorylated p38 mitogen-activated protein kinase ( MAPK ) .
Nuclear factor ( NF ) -κB expression was determined by muscle histopathology and immunohistochemistry .
HSYA attenuated pathologic changes instrike-induced soft tissue inflammation .
Treatment with HSYA also alleviated strike-induced increases in TNF-α , IL-1β , IL-6 , VCAM-1 , and ICAM-1mRNA levels and inhibited the increased activation of NF-κB and phosphorylation of @ @ @ @ @ @ @ findings suggest that HSYA effectively inhibits strike-induced inflammatory signal transduction in rats .

We examined the effect of hydroxysafflor yellow A (HSYA) on the inflammatory response to strike-induced acute soft tissue injury in rats. Soft tissue injury was induced in rat leg muscles using a strike hammer, followed by intraperitoneal administration of HSYA at 16, 32, or 64 mg/kg. After 24 h, the rats were anaesthetized, blood and muscle samples were taken. Plasma levels of interleukin (IL)-6, IL-1β, and tumour necrosis factor (TNF)-αwere measured by enzyme-linked immunosorbent assay. Total RNA and protein were isolated from muscle tissue to determine the mRNA levels of IL-6, IL-1β, TNF-α, vascular cell adhesion molecule (VCAM)-1, and intercellular adhesion molecule (ICAM)-1, and the protein level of phosphorylated p38 mitogen-activated protein kinase (MAPK). Nuclear factor (NF)-κB expression was determined by muscle histopathology and immunohistochemistry. HSYA attenuated pathologic changes instrike-induced soft tissue inflammation. Treatment with HSYA also alleviated strike-induced increases in TNF-α, IL-1β, IL-6, VCAM-1, and ICAM-1mRNA levels and inhibited the increased activation of NF-κB and phosphorylation of p38 MAPK in muscle tissue. These findings suggest that HSYA effectively inhibits strike-induced inflammatory signal transduction in rats.


greenmedinfo--2020-12-17--Yes, Bill Gates Said That. Here's the Proof

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greenmedinfo--2020-12-17--Hydroxysafflor yellow A cardioprotection in ischemia-reperfusion injury.

Hydroxysafflor yellow A ( HSYA ) is the main active component of Carthamus tinctorius L which has been used for hundreds of years in Chinese folk medicine in the treatment cardiovascular disease .
This study was designed to investigate whether HSYA exerts cardioprotection in ischemia-reperfusion ( I/R ) injury heart and the mechanisms involved .
The protective effect and mechanisms in myocardial ischemia reperfusion injury of HSYA was evaluated by hypoxia-recover ( H/R ) injury cell model which induced by hypoxia and recovered with oxygen in H9c2 cells .
PI3K/Akt and ERK as the reperfusion injury salvage kinase ( RISK @ @ @ @ @ @ @ ) were both examined .
In H/R cell model , HSYA significantly reduced dehydrogenase ( LDH ) , Caspase 3 level , alleviated oxidative stress injury and apoptosis , meanwhile restored mitochondrial energy metabolism .
Pretreatment with PI3K inhibitor ( LY294002 ) or hexokinase II inhibitor ( 3-BrPA ) , the protective effect of HSYA was significantly attenuated .
On the contrary , pretreatment with ERK inhibitor ( PD98059 ) , the protective effect of HSYA on myocardial cells was decreased slightly , not as significant as PI3K inhibitor or hexokinase II inhibitor @ @ @ @ @ @ @ myocardial protection by phosphorylation of GSK3-β , but the effect of HSYA on phosphorylation of GSK3-β is weakly , however the effect of HSYA on Akt and hexokinase II were significantly up-regulated .
Meanwhile , the phosphorylation of GSK3-β by HSYA was significantly reduced after gave the ERK inhibitor and had no significant difference betweenthe model group .
The cardioprotection effect of HSYA appears to be mainly mediated via the PI3K/Akt/hexokinase II .

Hydroxysafflor yellow A (HSYA) is the main active component of Carthamus tinctorius L which has been used for hundreds of years in Chinese folk medicine in the treatment cardiovascular disease. This study was designed to investigate whether HSYA exerts cardioprotection in ischemia-reperfusion (I/R) injury heart and the mechanisms involved. The protective effect and mechanisms in myocardial ischemia reperfusion injury of HSYA was evaluated by hypoxia-recover (H/R) injury cell model which induced by hypoxia and recovered with oxygen in H9c2 cells. PI3K/Akt and ERK as the reperfusion injury salvage kinase (RISK) pathway and Hexokinase II (HKII) were both examined. In H/R cell model, HSYA significantly reduced dehydrogenase (LDH), Caspase 3 level, alleviated oxidative stress injury and apoptosis, meanwhile restored mitochondrial energy metabolism. Pretreatment with PI3K inhibitor (LY294002) or hexokinase II inhibitor (3-BrPA), the protective effect of HSYA was significantly attenuated. On the contrary, pretreatment with ERK inhibitor (PD98059), the protective effect of HSYA on myocardial cells was decreased slightly, not as significant as PI3K inhibitor or hexokinase II inhibitor. ERK play a protective role in myocardial protection by phosphorylation of GSK3-β, but the effect of HSYA on phosphorylation of GSK3-β is weakly, however the effect of HSYA on Akt and hexokinase II were significantly up-regulated. Meanwhile, the phosphorylation of GSK3-β by HSYA was significantly reduced after gave the ERK inhibitor and had no significant difference betweenthe model group. The cardioprotection effect of HSYA appears to be mainly mediated via the PI3K/Akt/hexokinase II.


greenmedinfo--2020-12-17--Hydroxysafflor yellow A improved motor dysfunction in rotenone-induced Parkinson's disease model.

Dopamine D3 receptor ( DRD3 ) is diminished in patients of Parkinson 's disease ( PD ) .
Brain-derived neurotrophic factor ( BDNF ) is responsible for regulating expression of the DRD3 in the brain .
Our previous study showed that hydroxysafflor yellow A ( HSYA ) could increase BDNF content in the striatum of PD mice .
This experiment aimed to evaluate whether HSYA can improve the motor dysfunction induced by rotenone through regulating the BDNF/TrkB/DRD3 signaling pathway in mice .
Male C57/BL6 mice were intraperitoneally treated with HSYA .
Thirty minutes later , they were intragastrically administered with @ @ @ @ @ @ @ .
Pole , rotarod and open field tests were investigated at 28 d. Then , tyrosine hydroxylase ( TH ) in substantia nigra was observed by immunohistochemistry .
Dopamine content was detected by high-performance liquid chromatography .
The expressions of BDNF , phospho-tropomyosin-related kinase B ( p-TrkB ) , tropomyosin-related kinase B ( TrkB ) , phospho-phosphoinositide 3-kinase ( p-PI3K ) , phosphoinositide 3-kinase ( PI3K ) , phospho-protein kinase B ( p-AKT ) , protein kinase B ( AKT ) , and DRD3 were assayed by western blotting .
Behavioral tests showed @ @ @ @ @ @ @ However , treatment with HSYA improved motor dysfunction induced by rotenone .
HSYA treatment increased not only the number of TH-containing dopaminergic neurons in substantia nigra , but also the dopamine content in the striatum in PD mice .
Moreover , the expressions of BDNF , p-TrkB/TrkB , DRD3 , p-PI3K/PI3K , p-AKT/AKT were significantly increased in rotenone plus HSYA group .
Our results indicated that HSYA improved motor dysfunction in rotenone-induced PD model and the pharmacological action of HSYA was related to regulating BDNF/TrkB/DRD3 signaling pathway , at least , in part @

Dopamine D3 receptor (DRD3) is diminished in patients of Parkinson's disease (PD). Brain-derived neurotrophic factor (BDNF) is responsible for regulating expression of the DRD3 in the brain. Our previous study showed that hydroxysafflor yellow A (HSYA) could increase BDNF content in the striatum of PD mice. This experiment aimed to evaluate whether HSYA can improve the motor dysfunction induced by rotenone through regulating the BDNF/TrkB/DRD3 signaling pathway in mice. Male C57/BL6 mice were intraperitoneally treated with HSYA. Thirty minutes later, they were intragastrically administered with rotenone at a dose of 30 mg/kg. Pole, rotarod and open field tests were investigated at 28 d. Then, tyrosine hydroxylase (TH) in substantia nigra was observed by immunohistochemistry. Dopamine content was detected by high-performance liquid chromatography. The expressions of BDNF, phospho-tropomyosin-related kinase B (p-TrkB), tropomyosin-related kinase B (TrkB), phospho-phosphoinositide 3-kinase (p-PI3K), phosphoinositide 3-kinase (PI3K), phospho-protein kinase B (p-AKT), protein kinase B (AKT), and DRD3 were assayed by western blotting. Behavioral tests showed that rotenone-challenged mice displayed motor dysfunction. However, treatment with HSYA improved motor dysfunction induced by rotenone. HSYA treatment increased not only the number of TH-containing dopaminergic neurons in substantia nigra, but also the dopamine content in the striatum in PD mice. Moreover, the expressions of BDNF, p-TrkB/TrkB, DRD3, p-PI3K/PI3K, p-AKT/AKT were significantly increased in rotenone plus HSYA group. Our results indicated that HSYA improved motor dysfunction in rotenone-induced PD model and the pharmacological action of HSYA was related to regulating BDNF/TrkB/DRD3 signaling pathway, at least, in part.


greenmedinfo--2020-12-17--Hydroxysafflor yellow A alleviates lipopolysaccharide-induced acute respiratory distress syndrome.

Hydroxysafflor yellow A ( HSYA ) is an effective ingredient of the Chinese herb Carthamus tinctorius L. The present study investigated the protective effect of HSYA on lipopolysaccharide ( LPS ) -induced acute respiratory distress syndrome in mice , and the underlying mechanisms involved .
HSYA ( 14 , 28 , 56 mg/kg ) was intraperitoneally injected to mice once daily from day 1 to 10 after LPS administration .
HSYA attenuated the body weight loss , the augmented left index and the increase of pathologic changes in pulmonary inflammation caused by LPS .
Treatment with HSYA also alleviated increased @ @ @ @ @ @ @ ) -α , interleukin ( IL ) -1β , IL-6 , transforming growth factor ( TGF ) -β1 , collagen ( Col ) I , Col III , α-smooth muscle actin ( α-SMA ) , myeloid differentiation ( MD ) -2 , Toll-like receptor 4 ( TLR4 ) and cluster differentiation ( CD ) 14 at the mRNA ( RT-PCR ) and protein levels ( Western blot and enzyme-linked immuno sorbent assay ) .
Moreover , HSYA inhibited the elevated levels of nuclear factor ( NF ) -κB and α-SMA in lung tissue @ @ @ @ @ @ @ slight collagen deposition in pulmonary tissues ( Masson 's trichrome staining ) .
HSYA inhibited the specific binding of fluorescein isothiocyanate ( FITC ) -LPS on human lung epithelial cell line ( A549 ) or human umbilical vein cell line ( Eahy926 ) cells ( flow cytometry ) .
These findings suggested that HSYA has a protective effect on acute respiratory distress syndrome ( ARDS ) induced by LPS through blocking the TLR4/NF-κB pathway , and that the TLR4 receptor might be a target of HSYA on the cell membrane .

Hydroxysafflor yellow A (HSYA) is an effective ingredient of the Chinese herb Carthamus tinctorius L. The present study investigated the protective effect of HSYA on lipopolysaccharide (LPS)-induced acute respiratory distress syndrome in mice, and the underlying mechanisms involved. HSYA (14, 28, 56 mg/kg) was intraperitoneally injected to mice once daily from day 1 to 10 after LPS administration. HSYA attenuated the body weight loss, the augmented left index and the increase of pathologic changes in pulmonary inflammation caused by LPS. Treatment with HSYA also alleviated increased expressions of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, transforming growth factor (TGF)-β1, collagen (Col) I, Col III, α-smooth muscle actin (α-SMA), myeloid differentiation (MD)-2, Toll-like receptor 4 (TLR4) and cluster differentiation (CD)14 at the mRNA (RT-PCR) and protein levels(Western blot and enzyme-linked immuno sorbent assay). Moreover, HSYA inhibited the elevated levels of nuclear factor (NF)-κB and α-SMA in lung tissue (immunohistochemistry), and alleviated the slight collagen deposition in pulmonary tissues (Masson's trichrome staining). HSYA inhibited the specific binding of fluorescein isothiocyanate (FITC)-LPS on human lung epithelial cell line (A549) or human umbilical vein cell line (Eahy926) cells (flow cytometry). These findings suggested that HSYA has a protective effect on acute respiratory distress syndrome (ARDS) induced by LPS through blocking the TLR4/NF-κB pathway, and that the TLR4 receptor might be a target of HSYA on the cell membrane.


greenmedinfo--2020-12-18--Tanshinone IIA suppresses ovarian cancer growth through inhibiting malignant properties and angiogen

Tanshinone IIA suppresses ovarian cancer growth through inhibiting malignant properties and angiogenesis.

Background : In Chinese herbal medicine , Tanshinone IIA ( Tan-IIA ) is one of the main compounds extracted fromBunge .
Tan-IIA has been demonstrated to inhibit the growth of various tumors .
However , the detailed molecular and cellular mechanisms of the antitumor effect of Tan-IIA have yet to be fully illuminated .
Methods : A2780 and ID-8 were treated with 0 , 1.2 , 2.4 , 4.8 , or 9.6µg/mL Tan-IIA for 24 hours .
Cell counting Kit-8 assay and EdU staining were used to evaluate cell proliferation .
Terminal deoxynucleotidyl transferase dUTP nick end labeling ( TUNEL @ @ @ @ @ @ @ to analyze apoptosis .
Western blot was carried out to determine the protein levels .
Flow cytometry was used for cell cycle analysis .
The levels of mRNA expression were analyzed by real-time polymerase chain reaction .
The anti-tumor effect of Tan-IIA was observed in a tumor-bearing mouse model .
Results : Tan-IIA inhibited the proliferation of ovarian cancer cells in a dose-dependent manner by inducing G2/M phase arrest .
It also down-regulated B-cell lymphoma 2 ( Bcl-2 ) and up-regulated Bcl-2-associated X protein ( Bax ) in ovarian cancer cells to induce @ @ @ @ @ @ @ inhibiting focal adhesion kinase phosphorylation .
Tan-IIA significantly reduced vascular endothelial growth factor ( VEGF ) and cyclooxygenase-2 ( COX2 ) mRNA expression in ovarian cancer cells.
, Tan-IIA significantly inhibited tumor growth by inducing apoptosis and promoting anti-angiogenesis .
Conclusions : The results of this study shed light on the molecular and cellular mechanisms for the antitumor effect of Tan-IIA .

Background: In Chinese herbal medicine, Tanshinone IIA (Tan-IIA) is one of the main compounds extracted fromBunge. Tan-IIA has been demonstrated to inhibit the growth of various tumors. However, the detailed molecular and cellular mechanisms of the antitumor effect of Tan-IIA have yet to be fully illuminated.
Methods: A2780 and ID-8 were treated with 0, 1.2, 2.4, 4.8, or 9.6µg/mL Tan-IIA for 24 hours. Cell counting Kit-8 assay and EdU staining were used to evaluate cell proliferation. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and flow cytometry were performed to analyze apoptosis. Western blot was carried out to determine the protein levels. Flow cytometry was used for cell cycle analysis. The levels of mRNA expression were analyzed by real-time polymerase chain reaction. The anti-tumor effect of Tan-IIA was observed in a tumor-bearing mouse model.
Results: Tan-IIA inhibited the proliferation of ovarian cancer cells in a dose-dependent manner by inducing G2/M phase arrest. It also down-regulated B-cell lymphoma 2 (Bcl-2) and up-regulated Bcl-2-associated X protein (Bax) in ovarian cancer cells to induce apoptosis, and suppressed cell migration by inhibiting focal adhesion kinase phosphorylation. Tan-IIA significantly reduced vascular endothelial growth factor (VEGF) and cyclooxygenase-2 (COX2) mRNA expression in ovarian cancer cells., Tan-IIA significantly inhibited tumor growth by inducing apoptosis and promoting anti-angiogenesis.
Conclusions: The results of this study shed light on the molecular and cellular mechanisms for the antitumor effect of Tan-IIA.


greenmedinfo--2020-12-18--Protocatechuic aldehyde from Salvia miltiorrhiza exhibits an anti-inflammatory effect through inhibi

Protocatechuic aldehyde from Salvia miltiorrhiza exhibits an anti-inflammatory effect through inhibiting MAPK signalling pathway.

BACKGROUND : The aerial parts of Salvia miltiorrhiza , which was considered to be the waste part and discarded during the root harvest , is rich in protocatechuic aldehyde ( PAI ) .
This study investigated the health-promoting effects of extracts and PAI from the aerial parts of Salvia miltiorrhiza , including its anti-inflammatory effects and the underlying mechanisms of action in vitro and in vivo .
METHOD : Purification of the sample paste of Salvia miltiorrhiza was accomplished using HPLC analysis .
TheMTT ( Methylthiazolyldiphenyl-tetrazolium bromide ) assay was employed to determine the cell viability .
The production of @ @ @ @ @ @ @ .
The histopathological analysis was used to analyse the lungs and livers of mice treated with PAI .
Western blot was performed to reveal the mechanism of PAI in anti-inflammatory .
RESULTS : The extracts and PAI from the aerial parts of Salvia miltiorrhiza inhibited TNF-α , IL-6 production and promoted the production of IL-10 in vivo in mice and in vitro in the macrophage cell line RAW264.7 .
NF-κB and MAPKs kinase phosphorylation were also suppressed by PAI in vivo and in vitro , indicating that PAI exhibited an anti-inflammatory effect .
@ @ @ @ @ @ @ aerial parts of Salvia miltiorrhiza extract may serve as potential protective agents for inflammatory .

BACKGROUND: The aerial parts of Salvia miltiorrhiza, which was considered to be the waste part and discarded during the root harvest, is rich in protocatechuic aldehyde (PAI). This study investigated the health-promoting effects of extracts and PAI from the aerial parts of Salvia miltiorrhiza, including its anti-inflammatory effects and the underlying mechanisms of action in vitro and in vivo.
METHOD: Purification of the sample paste of Salvia miltiorrhiza was accomplished using HPLC analysis. TheMTT (Methylthiazolyldiphenyl-tetrazolium bromide) assay was employed to determine the cell viability. The production of inflammatory factors was detected by ELISA assays. The histopathological analysis was used to analyse the lungs and livers of mice treated with PAI. Western blot was performed to reveal the mechanism of PAI in anti-inflammatory.
RESULTS: The extracts and PAI from the aerial parts of Salvia miltiorrhiza inhibited TNF-α, IL-6 production and promoted the production of IL-10 in vivo in mice and in vitro in the macrophage cell line RAW264.7. NF-κB and MAPKs kinase phosphorylation were also suppressed by PAI in vivo and in vitro, indicating that PAI exhibited an anti-inflammatory effect.
CONCLUSION: These findings suggest that the aerial parts of Salvia miltiorrhiza extract may serve as potential protective agents for inflammatory.


greenmedinfo--2020-12-18--C. tinctorius extract prevented the LPS-induced apoptotic response through IGF-I pathway.

Carthamus tinctorius L. ( Compositae ) is used in Chinese medicine to treat heart disease and inflammation .
In our previous study , we found that C. tinctorius L. inhibited lipopolysaccharides ( LPS ) -induced tumor necrosis factor-alpha ( TNF-α ) activation , JNK expression , and apoptosis in H9c2 cardiomyoblast cells .
The present study was performed to investigate the protective effect of C. tinctorius extract ( CTF ) on LPS-challenged H9c2 myocardioblast cell and to explore the possible underlying mechanism .
Cell viability assay showed that LPS treatment decreased the cell viability of H9c2 cell , whereas CTF @ @ @ @ @ @ @ manner , especially in the LPS + CTF 25 ( μg/mL ) group .
LPS treatment-induced apoptosis was determined by transferase-mediated dUTP nick end labeling assay , and by Western blot .
LPS-induced apoptotic bodies were decreased following CTF treatment .
Expression of TNF-α , FAS-L , FAS , FADD , caspase-8 , BID , and t-BID was significantly increased in LPS-treated H9c2 cells .
In contrast , it was significantly suppressed by the administration of CTF extract .
In addition , CTF treatment activates antiapoptotic proteins , Bcl-2 and p-Bad , and @ @ @ @ @ @ @ caspase-3 , and apoptosis-inducing factor expression .
Furthermore , CTF exerted cytoprotective effects by activating insulin-like growth factor-I ( IGF-I ) signaling pathway leading to downregulation of the apoptotic proteins involved in FAS death receptor pathway .
In addition , AG1024 and IGF-I receptor ( IGF-IR ) inhibitor and siRNA silencing reverses the effect of CTF implying that CTF functions through the IGF-IR pathway to inhibit LPS-induced H9c2 apoptosis .
These results suggest that treatment with CTF extract prevented the LPS-induced apoptotic response through IGF-I pathway .

Carthamus tinctorius L. (Compositae) is used in Chinese medicine to treat heart disease and inflammation. In our previous study, we found that C. tinctorius L. inhibited lipopolysaccharides (LPS)-induced tumor necrosis factor-alpha (TNF-α) activation, JNK expression, and apoptosis in H9c2 cardiomyoblast cells. The present study was performed to investigate the protective effect of C. tinctorius extract (CTF) on LPS-challenged H9c2 myocardioblast cell and to explore the possible underlying mechanism. Cell viability assay showed that LPS treatment decreased the cell viability of H9c2 cell, whereas CTF treatment reversed LPS cytotoxicity in a dose-dependent manner, especially in the LPS + CTF 25 (μg/mL) group. LPS treatment-induced apoptosis was determined by transferase-mediated dUTP nick end labeling assay, and by Western blot. LPS-induced apoptotic bodies were decreased following CTF treatment. Expression of TNF-α, FAS-L, FAS, FADD, caspase-8, BID, and t-BID was significantly increased in LPS-treated H9c2 cells. In contrast, it was significantly suppressed by the administration of CTF extract. In addition, CTF treatment activates antiapoptotic proteins, Bcl-2 and p-Bad, and downregulates Bax, cytochrome-c, caspase-9, caspase-3, and apoptosis-inducing factor expression. Furthermore, CTF exerted cytoprotective effects by activating insulin-like growth factor-I (IGF-I) signaling pathway leading to downregulation of the apoptotic proteins involved in FAS death receptor pathway. In addition, AG1024 and IGF-I receptor (IGF-IR) inhibitor and siRNA silencing reverses the effect of CTF implying that CTF functions through the IGF-IR pathway to inhibit LPS-induced H9c2 apoptosis. These results suggest that treatment with CTF extract prevented the LPS-induced apoptotic response through IGF-I pathway.


greenmedinfo--2020-12-19--Grape seed extract may exert anti-tumorigenic effects on chemo-resistant OVCAR-3 ovarian cancer cell

Grape seed extract may exert anti-tumorigenic effects on chemo-resistant OVCAR-3 ovarian cancer cells.

Background and purpose : Ovarian cancer is the deadliest cancer in women .
The main challenge in the inhibition of ovarian cancer cells is chemo-resistance .
Seeking to overcome this issue , several strategies have been suggested , including the administration of natural products .
Grape seed extract ( GSE ) is a good source of polyphenols and its anticancer effects have been reported by many studies .
In this study we aimed to evaluate the effects of GSE on OVCAR-3 , a chemo-resistant ovarian cancer line .
Experimental approach : OVCAR-3 cells were treated with GSE ( 71μg/mL ) @ @ @ @ @ @ @ and cell apoptosis were measured by MTT and flow cytometry .
The real-time polymerase chain reaction was used to determine the expression of genes involved in the cell cycle ( PTEN , DACT1 , AKT , MTOR , GSK3B , C-MYC , CCND1 , and CDK4 ) and apoptosis ( BAX , BCl2 , CASP3 , 8 and 9 ) .
The expression of CASP3 protein was evaluated by the CASP3 assay .
Findings / Results : The results showed that treatment of OVCAR-3 cells with GSE , increased the expression level of @ @ @ @ @ @ @ as well as apoptotic genes , CASP3 , 8 , and 9 ( < 0.001 ) .
Also , the induction of tumor suppressor genes expression was associated with an increase in the expression of BAX/BCL2 gene ratio as pro- and anti-apoptotic genes .
The expression of the genes involved in the cell cycle , CCND1 and CDK4 , was inhibited ( < 0.001 ) .
The results indicated that GSE induced cell apoptosis in a time-dependent manner ( < 0.001 ) .
Also , the GSE treatment resulted in the CASP3 protein @ @ @ @ @ @ @ and implications : According to the results of this study , GSE may exert anti-tumorigenic effects on chemo-resistant OVCAR-3 ovarian cancer cells which might be mediated by the expression of tumor suppressor genes that interact with cell signaling pathways , cell cycle , and cell apoptosis .
Hence , the consumption of GSE extract during chemotherapy may overcome part of chemo-resistance in ovarian cancer .

Background and purpose: Ovarian cancer is the deadliest cancer in women. The main challenge in the inhibition of ovarian cancer cells is chemo-resistance. Seeking to overcome this issue, several strategies have been suggested, including the administration of natural products. Grape seed extract (GSE) is a good source of polyphenols and its anticancer effects have been reported by many studies. In this study we aimed to evaluate the effects of GSE on OVCAR-3, a chemo-resistant ovarian cancer line.
Experimental approach: OVCAR-3 cells were treated with GSE (71μg/mL) for 24 and 48 h. Cell viability and cell apoptosis were measured by MTT and flow cytometry. The real-time polymerase chain reaction was used to determine the expression of genes involved in the cell cycle (PTEN, DACT1, AKT, MTOR, GSK3B, C-MYC, CCND1, and CDK4) and apoptosis (BAX, BCl2, CASP3, 8 and 9). The expression of CASP3 protein was evaluated by the CASP3 assay.
Findings / Results: The results showed that treatment of OVCAR-3 cells with GSE, increased the expression level of PTEN and DACT1 tumor suppressor genes, as well as apoptotic genes, CASP3, 8, and 9 (<0.001). Also, the induction of tumor suppressor genes expression was associated with an increase in the expression of BAX/BCL2 gene ratio as pro- and anti-apoptotic genes. The expression of the genes involved in the cell cycle, CCND1 and CDK4, was inhibited (<0.001). The results indicated that GSE induced cell apoptosis in a time-dependent manner (<0.001). Also, the GSE treatment resulted in the CASP3 protein expression (<0.001).
Conclusion and implications: According to the results of this study, GSE may exert anti-tumorigenic effects on chemo-resistant OVCAR-3 ovarian cancer cells which might be mediated by the expression of tumor suppressor genes that interact with cell signaling pathways, cell cycle, and cell apoptosis. Hence, the consumption of GSE extract during chemotherapy may overcome part of chemo-resistance in ovarian cancer.


greenmedinfo--2020-12-19--Polyphenols in the treatment of inflammatory bowel diseases.

Inflammatory bowel diseases ( IBD ) , including Crohn 's disease ( CD ) and ulcerative colitis ( UC ) @ @ @ @ @ The exact etiology of IBD is not well elucidated , however it is defined as @ @ @ @ @ addition , IBD carries the risk of serious complications and increases the risk of colorectal @ @ @ @ @ recent years , an increased rate of IBD cases has been noted .
So far @ @ @ @ @ and well-defined therapy for IBD , and currently available drugs mainly provide symptomatic treatment .
@ @ @ @ @ not always bring the expected benefits , moreover , it is often associated with unpleasant @ @ @ @ @ some research have been focused on unconventional forms of IBD treatment , testing therapies based @ @ @ @ @ polyphenols , as well as polyphenol-rich preparations and extracts are also valuable in IBD treatment @ @ @ @ @ bactericidal activity .
Moreover , described here results of clinical trials suggest that polyphenols can @ @ @ @ @ of IBD .

Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), are chronic diseases. The exact etiology of IBD is not well elucidated, however it is defined as a multifactorial disease. In addition, IBD carries the risk of serious complications and increases the risk of colorectal cancer. Also, in recent years, an increased rate of IBD cases has been noted. So far, there is no effective and well-defined therapy for IBD, and currently available drugs mainly provide symptomatic treatment. Unfortunately, conventional treatment does not always bring the expected benefits, moreover, it is often associated with unpleasant side effects. Currently, some research have been focused on unconventional forms of IBD treatment, testing therapies based on natural products. Individual polyphenols, as well as polyphenol-rich preparations and extracts are also valuable in IBD treatment through antioxidant, anti-inflammatory and bactericidal activity. Moreover, described here results of clinical trials suggest that polyphenols can alleviate symptoms and prevent recurrence of IBD.


greenmedinfo--2020-12-19--The role of EGCG in breast cancer prevention and therapy.

BACKGROUND : Breast cancer is the most frequent cancer in women .
Green tea has been studied for breast cancer chemopreventive and possibly chemotherapeutic effects due to its high content in polyphenolic compounds , including epigallocatechin-3-gallate ( EGCG ) .
METHOD : This review is based on a literature research that included papers registered on the Medline database .
The research was conducted through PubMed , with the application of the following query : '' EGCG '' AND 'breast cancer '' .
The result was a total of 88 articles in which this review stands on .
RESULTS : In @ @ @ @ @ @ @ properties , depending on the concentration and exposure time .
EGCG blocks cell cycle progression and modulates signaling pathways that affects cell proliferation and differentiation .
EGCG also induces apoptosis , negatively modulates different steps involved in metastasis and targets angiogenesis by inhibiting VEGF transcription .
In vivo , investigations have shown that oral administration of EGCG results in reduction of tumor growth and in antimetastatic and antiangiogenic effects in animal xenograft and allograft models .
DISCUSSION : Much remains unknown about the molecular mechanisms involved in the protective effects of EGCG on @ @ @ @ @ @ @ studies in vivo are necessary to determine the potential toxicity of EGCG at higher doses and to elucidate its interactions with other drugs .
CONCLUSION : A protective effect of EGCG has been shown in different experimental models and under different experimental conditions , suggesting clinical implications of EGCG for breast cancer prevention and therapy .
The data presented in this review support the importance of further investigations .

BACKGROUND: Breast cancer is the most frequent cancer in women. Green tea has been studied for breast cancer chemopreventive and possibly chemotherapeutic effects due to its high content in polyphenolic compounds, including epigallocatechin-3-gallate (EGCG).
METHOD: This review is based on a literature research that included papers registered on the Medline database. The research was conducted through PubMed, with the application of the following query:"EGCG"AND 'breast cancer". The result was a total of 88 articles in which this review stands on.
RESULTS: In vitro, EGCG shows antioxidant or pro-oxidant properties, depending on the concentration and exposure time. EGCG blocks cell cycle progression and modulates signaling pathways that affects cell proliferation and differentiation. EGCG also induces apoptosis, negatively modulates different steps involved in metastasis and targets angiogenesis by inhibiting VEGF transcription. In vivo, investigations have shown that oral administration of EGCG results in reduction of tumor growth and in antimetastatic and antiangiogenic effects in animal xenograft and allograft models.
DISCUSSION: Much remains unknown about the molecular mechanisms involved in the protective effects of EGCG on mammary carcinogenesis. In addition, more studies in vivo are necessary to determine the potential toxicity of EGCG at higher doses and to elucidate its interactions with other drugs.
CONCLUSION: A protective effect of EGCG has been shown in different experimental models and under different experimental conditions, suggesting clinical implications of EGCG for breast cancer prevention and therapy. The data presented in this review support the importance of further investigations.


greenmedinfo--2020-12-19--Resveratrol confers neuroprotection against high-fat diet in a mouse model of Alzheimer's disease.

Cumulative evidence indicates that excessive consumption of calories from saturated fat contributes to the development of Alzheimer 's disease ( AD ) .
Here we assess the triggering and progression of AD pathology induced by a high-fat diet ( HFD ) , and the effects of resveratrol , a polyphenol found in common dietary sources with pleiotropic neuroprotective activities .
Over 16 weeks , male wild type ( WT ) and AD transgenic 5XFAD mice were fed a control diet , HFD ( 60 % kcal from fat ) , or HFD supplemented with 0.1 % resveratrol .
Resveratrol protected @ @ @ @ @ @ @ and prevented memory loss in 5XFAD mice .
Resveratrol also reduced the amyloid burden aggravated by HFD in 5XFAD , and protected against HFD-induced tau pathology in both WT and 5XFAD strains .
At the mechanistic level , resveratrol inhibited the HFD-increased amyloidogenic processing of the amyloid precursor protein in both strains ; it also restored abnormal high levels in the proteolytic activity of the ubiquitin-proteasome system induced by HFD , suggesting the presence of a compensatory mechanism to counteract the accumulation of aberrant proteins .
Thus , our data suggest that resveratrol @ @ @ @ @ @ @ in the brain and may be a potential therapeutic agent against obesity-related disorders and AD pathology .

Cumulative evidence indicates that excessive consumption of calories from saturated fat contributes to the development of Alzheimer's disease (AD). Here we assess the triggering and progression of AD pathology induced by a high-fat diet (HFD), and the effects of resveratrol, a polyphenol found in common dietary sources with pleiotropic neuroprotective activities. Over 16 weeks, male wild type (WT) and AD transgenic 5XFAD mice were fed a control diet, HFD (60% kcal from fat), or HFD supplemented with 0.1% resveratrol. Resveratrol protected against HFD-induced memory loss in WT mice and prevented memory loss in 5XFAD mice. Resveratrol also reduced the amyloid burden aggravated by HFD in 5XFAD, and protected against HFD-induced tau pathology in both WT and 5XFAD strains. At the mechanistic level, resveratrol inhibited the HFD-increased amyloidogenic processing of the amyloid precursor protein in both strains; it also restored abnormal high levels in the proteolytic activity of the ubiquitin-proteasome system induced by HFD, suggesting the presence of a compensatory mechanism to counteract the accumulation of aberrant proteins. Thus, our data suggest that resveratrol can correct the harmful effects of HFD in the brain and may be a potential therapeutic agent against obesity-related disorders and AD pathology.


greenmedinfo--2020-12-19--Can natural polyphenols help in reducing cytokine storm in COVID-19 patients?

SARS-CoV-2 first emerged in China during late 2019 and rapidly spread all over the world .
Alterations in the inflammatory cytokines pathway represent a strong signature during SARS-COV-2 infection and correlate with poor prognosis and severity of the illness .
The hyper-activation of the immune system results in an acute severe systemic inflammatory response named cytokine release syndrome ( CRS ) .
No effective prophylactic or post-exposure treatments are available , although some anti-inflammatory compounds are currently in clinical trials .
Studies of plant extracts and natural compounds show that polyphenols can play a beneficial role in the prevention and @ @ @ @ @ @ @ inflammation .
The aim of this manuscript is to review the published background on the possible effectiveness of polyphenols to fight SARS-COV-2 infection , contributing to the reduction of inflammation .
Here , some of the anti-inflammatory therapies are discussed and although great progress has been made though this year , there is no proven cytokine blocking agents for COVID currently used in clinical practice .
In this regard , bioactive phytochemicals such as polyphenols may become promising tools to be used as adjuvants in the treatment of SARS-CoV-2 infection .
Such nutrients @ @ @ @ @ @ @ associated to classical anti-inflammatory drugs , could help in reducing the inflammation in patients with COVID-19 .

SARS-CoV-2 first emerged in China during late 2019 and rapidly spread all over the world. Alterations in the inflammatory cytokines pathway represent a strong signature during SARS-COV-2 infection and correlate with poor prognosis and severity of the illness. The hyper-activation of the immune system results in an acute severe systemic inflammatory response named cytokine release syndrome (CRS). No effective prophylactic or post-exposure treatments are available, although some anti-inflammatory compounds are currently in clinical trials. Studies of plant extracts and natural compounds show that polyphenols can play a beneficial role in the prevention and the progress of chronic diseases related to inflammation. The aim of this manuscript is to review the published background on the possible effectiveness of polyphenols to fight SARS-COV-2 infection, contributing to the reduction of inflammation. Here, some of the anti-inflammatory therapies are discussed and although great progress has been made though this year, there is no proven cytokine blocking agents for COVID currently used in clinical practice. In this regard, bioactive phytochemicals such as polyphenols may become promising tools to be used as adjuvants in the treatment of SARS-CoV-2 infection. Such nutrients, with anti-inflammatory and antioxidant properties, associated to classical anti-inflammatory drugs, could help in reducing the inflammation in patients with COVID-19.


greenmedinfo--2020-12-18--Polyphenol from millet bran increases the sensitivity of colorectal cancer cells to oxaliplatin by b

Polyphenol from millet bran increases the sensitivity of colorectal cancer cells to oxaliplatin by blocking the ganglioside GM3 catabolism.

Colorectal cancer ( CRC ) is an aggressive malignancy with very limited therapeutic approaches .
Drug resistance develops as a frequent characteristic in many patients with CRC , which leads to a decrease in the therapeutic efficacy of anticancer agents .
Our previous evidences showed that bound polyphenol from millet bran ( BPIS ) possesses the potential of inhibiting cancer cell proliferation , and its main anticancer components are ferulic acid ( FA ) and p-coumaric acid ( p-CA ) .
In the present study , we found that BPIS significantly increases the sensitivity of human drug-resistant CRC cell line @ @ @ @ @ @ @ commonly used chemotherapy drug against CRC .
Mechanistically , we indicated that BPIS significantly impairs the expression of a gene encoding multidrug resistance protein 1 ( MDR1 ) , a well-known permeability glycoprotein ( P-gp ) , by preventing ganglioside GM3 catabolism .
Neuraminidase 3 ( NEU3 ) is a key enzyme catalyzing the conversion of ganglioside GM3 to ceramide trihexosides ( Gb3 ) , whose expression is increased in drug-resistant HCT-116/L cells .
BPIS treatment increased GM3 level , but reduced Gb3 and P-gp levels by inhibiting NEU3 expression , which subsequently @ @ @ @ @ @ @ cells to OXA .
These findings reveal that BPIS increases the chemo-sensitivity by remodeling NEU3-mediated ganglioside GM3 catabolism , and it may be applied as a novel drug for facilitating the effectiveness of chemotherapeutic agents in CRC .

Colorectal cancer (CRC) is an aggressive malignancy with very limited therapeutic approaches. Drug resistance develops as a frequent characteristic in many patients with CRC, which leads to a decrease in the therapeutic efficacy of anticancer agents. Our previous evidences showed that bound polyphenol from millet bran (BPIS) possesses the potential of inhibiting cancer cell proliferation, and its main anticancer components are ferulic acid (FA) and p-coumaric acid (p-CA). In the present study, we found that BPIS significantly increases the sensitivity of human drug-resistant CRC cell line to oxaliplatin (OXA), a commonly used chemotherapy drug against CRC. Mechanistically, we indicated that BPIS significantly impairs the expression of a gene encoding multidrug resistance protein 1 (MDR1), a well-known permeability glycoprotein (P-gp), by preventing ganglioside GM3 catabolism. Neuraminidase 3 (NEU3) is a key enzyme catalyzing the conversion of ganglioside GM3 to ceramide trihexosides (Gb3), whose expression is increased in drug-resistant HCT-116/L cells. BPIS treatment increased GM3 level, but reduced Gb3 and P-gp levels by inhibiting NEU3 expression, which subsequently boosted the chemotherapy sensitivity of drug-resistant HCT-116/L cells to OXA. These findings reveal that BPIS increases the chemo-sensitivity by remodeling NEU3-mediated ganglioside GM3 catabolism, and it may be applied as a novel drug for facilitating the effectiveness of chemotherapeutic agents in CRC.


greenmedinfo--2020-12-18--Skip Sweet Treats to Avoid Holiday Blues


greenmedinfo--2020-12-18--Researchers Discover Why Gum Disease Causes Heart Disease


greenmedinfo--2020-12-18--Eugenol attenuates inflammatory response and enhances barrier function during lipopolysaccharide-ind

Eugenol attenuates inflammatory response and enhances barrier function during lipopolysaccharide-induced inflammation.

Eugenol ( 4-allyl-2-methoxyphenol ) is an essential oil component , possessing antimicrobial , anti-inflammatory , and antioxidative properties ; however , the effect of eugenol on porcine gut inflammation has not yet been investigated .
In this study , an in vitro lipopolysaccharide ( LPS ) -induced inflammation model in porcine intestinal epithelial cells ( IPEC-J2 ) has been set up .
Cells were pretreated with 100μM ( 16.42 mg/L ) eugenol for 2 h followed by 10 μg/mL LPS stimulation for 6 h. Proinflammatory cytokine secretion ; reactive oxygen species ; gene expression of proinflammatory cytokines , tight junction @ @ @ @ @ @ @ expression and distribution of zonula occludens-1 ( ZO-1 ) ; transepithelial electrical resistance ( TEER ) ; and cell permeability were measured to investigate the effect of eugenol on inflammatory responses and gut barrier function .
The results showed that eugenol pretreatment significantly suppressed the LPS-stimulated interleukin-8 level and the mRNA abundance of tumor necrosis factor-α and restored the LPS-stimulated decrease of the mRNA abundance of tight junction proteins , such as ZO-1 and occludin , and the mRNA abundance of nutrient transporters , such as B0 1 system ASC sodium-dependent neutral amino @ @ @ @ @ @ @ 1 , excitatory amino acid transporter 1 , and peptide transporter 1 .
In addition , eugenol improved the expression and even redistribution of ZO-1 and tended to increase TEER value and maintained the barrier integrity .
In conclusion , a low dose of eugenol attenuated inflammatory responses andenhanced selectively permeable barrier function during LPS-induced inflammation in the IPEC-J2 cell line .

Eugenol (4-allyl-2-methoxyphenol) is an essential oil component, possessing antimicrobial, anti-inflammatory, and antioxidative properties; however, the effect of eugenol on porcine gut inflammation has not yet been investigated. In this study, an in vitro lipopolysaccharide (LPS)-induced inflammation model in porcine intestinal epithelial cells (IPEC-J2) has been set up. Cells were pretreated with 100μM (16.42 mg/L) eugenol for 2 h followed by 10 μg/mL LPS stimulation for 6 h. Proinflammatory cytokine secretion; reactive oxygen species; gene expression of proinflammatory cytokines, tight junction proteins, and nutrient transporters; the expression and distribution of zonula occludens-1 (ZO-1);transepithelial electrical resistance (TEER); and cell permeability were measured to investigate the effect of eugenol on inflammatory responses and gut barrier function. The results showed that eugenol pretreatment significantly suppressed the LPS-stimulated interleukin-8 level and the mRNA abundance of tumor necrosis factor-α and restored the LPS-stimulated decrease of the mRNA abundance of tight junction proteins, such as ZO-1 and occludin, and the mRNA abundance of nutrient transporters, such as B0 1 system ASC sodium-dependent neutral amino acid exchanger 2, sodium-dependent glucose transporter 1, excitatory amino acid transporter 1, and peptide transporter 1. In addition, eugenol improved the expression and even redistribution of ZO-1 and tended to increase TEER value and maintained the barrier integrity. In conclusion, a low dose of eugenol attenuated inflammatory responses andenhanced selectively permeable barrier function during LPS-induced inflammation in the IPEC-J2 cell line.


greenmedinfo--2020-12-18--Eugenol improves insulin secretion and content of pancreatic islets from male mouse.

Glucose homeostasis is required for control of insulin secretion .
Phenolic compounds improved glucose-stimulated insulin secretion ( GSIS ) .
Eugenol is a phenolic compound that may increase GSIS .
So , it was decided to investigate the effect of eugenol on the insulin secretion and content of pancreatic islets from the male mice .
In this experimental study , 3-month-old NMRI mice ( 20-25 g ) were prepared .
The pancreatic islets of Langerhans were isolated using the collagenase digestion method and divided into 12 groups : glucose 2.8 , 5.6 , and 16.7 mM , glucose 2.8 mM @ @ @ @ @ @ @ 200 M , glucose 5.6 mM + eugenol 50 , 100 , and 200 M , and glucose 16.7 mM + eugenol 50 , 100 , and 200 M. The islet 's insulin secretion and content were measured after 1 hour and 24 hours incubation at 37°C , respectively , by the ELISA assays method and related commercial kit .
Present results showed that all doses of eugenol increased islet 's insulin secretion and content in the medium containing glucose concentrations 2.8 , 5.6 , and 16.7 mM ( < 0.05 ) .
@ @ @ @ @ @ @ compound increased insulin secretion and content of pancreatic islets .
The moderate dose of this compound enhanced insulin secretion during hypo- and hyperglycemic conditions , as well as a high dose of eugenol , increased insulin content .
Finally , present research suggested that the administration of eugenol 100 M was suitable for the early stage of T2DM as well as eugenol 200 M for the advanced stage of this disease .

Glucose homeostasis is required for control of insulin secretion. Phenolic compounds improved glucose-stimulated insulin secretion (GSIS). Eugenol is a phenolic compound that may increase GSIS. So, it was decided to investigate the effect of eugenol on the insulin secretion and content of pancreatic islets from the male mice. In this experimental study, 3-month-old NMRI mice (20-25 g) were prepared. The pancreatic islets of Langerhans were isolated using the collagenase digestion method and divided into 12 groups: glucose 2.8, 5.6, and 16.7 mM, glucose 2.8 mM + eugenol 50, 100, and 200 M, glucose 5.6 mM + eugenol 50, 100, and 200 M, and glucose 16.7 mM + eugenol 50, 100, and 200 M. The islet's insulin secretion and content were measured after 1 hour and 24 hours incubation at 37°C, respectively, by the ELISA assays method and related commercial kit. Present results showed that all doses of eugenol increased islet's insulin secretion and content in the medium containing glucose concentrations 2.8, 5.6, and 16.7 mM (<0.05). In conclusion, eugenol as a phenolic compound increased insulin secretion and content of pancreatic islets. The moderate dose of this compound enhanced insulin secretion during hypo- and hyperglycemic conditions, as well as a high dose of eugenol, increased insulin content. Finally, present research suggested that the administration of eugenol 100 M was suitable for the early stage of T2DM as well as eugenol 200 M for the advanced stage of this disease.


greenmedinfo--2020-12-18--Eugenol and capsaicin exhibit anti-metastatic activity via modulating TGF-β signaling in gastric car

Eugenol and capsaicin exhibit anti-metastatic activity via modulating TGF-β signaling in gastric carcinoma.

The transforming growth factor-β ( TGF-β ) signaling is considered to be a key player in gastric cancer metastasis , @ @ @ @ @ TGF-β/SMAD4 signaling pathway may be a novel strategy for therapeutic interventions in cancer .
Here @ @ @ @ @ two phytochemicals , eugenol and capsaicin , has been studied , and their potential to @ @ @ @ @ in gastric cancer cells .
Both the phytochemicals exhibited anti-metastatic activity by inhibiting the TGF-β @ @ @ @ @ or P53 , with capsaicin proving to be more potent than eugenol .
However , @ @ @ @ @ effect of capsaicin on the TGF-β signaling pathway and metastasis was found to be dependent @ @ @ @ @ validated in SMAD4-knocked down AGS cell and SMAD4-null SW620 cell line .
Furthermore , the @ @ @ @ @ TGF-β receptor inhibitor LY2109761 confirmed that the anti-metastatic activity of eugenol is partially and that @ @ @ @ @ through the TGF-β signaling pathway .
Identifying phytochemicals with the potential to inhibit cancer metastasis @ @ @ @ @ pathway has immense scope for developing a therapeutic strategy against cancer metastasis .

The transforming growth factor-β (TGF-β) signaling is considered to be a key player in gastric cancer metastasis, and the inhibition of the TGF-β/SMAD4 signaling pathway may be a novel strategy for therapeutic interventions in cancer. Here, the anti-metastatic activity of two phytochemicals, eugenol and capsaicin, has been studied, and their potential to antagonize TGF-β has been investigated in gastric cancer cells. Both the phytochemicals exhibited anti-metastatic activity by inhibiting the TGF-β signaling pathway independent of P21 or P53, with capsaicin proving to be more potent than eugenol. However, unlike eugenol, the inhibitory effect of capsaicin on the TGF-β signaling pathway and metastasis was found to be dependent on SMAD4, which was validated in SMAD4-knocked down AGS cell and SMAD4-null SW620 cell line. Furthermore, the use of recombinant TGF-β and TGF-β receptor inhibitor LY2109761 confirmed that the anti-metastatic activity of eugenol is partially and that of capsaicin is principally mediated through the TGF-β signaling pathway. Identifying phytochemicals with the potential to inhibit cancer metastasis by targeting the TGF-β signaling pathway has immense scope for developing a therapeutic strategy against cancer metastasis.