greenmedinfo--2020-12-16--Hydroxysafflor yellow A attenuates high glucose-induced pancreatic β-cells oxidative damage.

Pancreaticβ-cells apoptosis and dysfunction induced by glucose toxicity were attributed to the formation of excess oxidative damage .
Some studies have found that hydroxysafflor yellow A has strong effects to scavenge oxidative stress and inhibit apoptosis .
In order to explore the influence of HSYA on oxidative stress induced by high glucose and the potential mechanisms , we set up a high glucose damage model and induced oxidative stress in INS-1 rat insulinoma cells .
N-acetylcysteine was added as a group of oxidative stress scavenger .
After 72 h of cultivation , the related indexes of oxidative stress ( reactive @ @ @ @ @ @ @ , lipid peroxidation , and superoxide dismutase ) , apoptosis ( caspase3 , parp ) and the function of glucose stimulated insulin secretion were determined .
In addition , the signaling pathway proteins of C-Jun NH2 -terminal kinases ( JNK ) , phosphorylated JNK , C-jun , phosphorylated C-jun were evaluated .
Fluorescence microscopy , qRT-PCR , western blotting were the main methods used in the experiment .
Our results showed that hydroxysafflor yellow A reduced pancreatic β-cells apoptosis by attenuating oxidative damage , and JNK/c-Jun signaling pathway was involved .
It indicated @ @ @ @ @ @ @ of HSYA on oxidative stress induced by high glucose , and provide important basis for using HSYA in diabetic prevention and therapy .

Pancreaticβ-cells apoptosis and dysfunction induced by glucose toxicity were attributed to the formation of excess oxidative damage. Some studies have found that hydroxysafflor yellow A has strong effects to scavenge oxidative stress and inhibit apoptosis. In order to explore the influence of HSYA on oxidative stress induced by high glucose and the potential mechanisms, we set up a high glucose damage model and induced oxidative stress in INS-1 rat insulinoma cells. N-acetylcysteine was added as a group of oxidative stress scavenger. After 72 h of cultivation, the related indexes of oxidative stress(reactive oxygen species, catalase, glutathione peroxidase, lipid peroxidation, and superoxide dismutase), apoptosis (caspase3, parp) and the function of glucose stimulated insulin secretion were determined. In addition, the signaling pathway proteins of C-Jun NH2 -terminal kinases (JNK), phosphorylated JNK, C-jun, phosphorylated C-jun were evaluated. Fluorescence microscopy, qRT-PCR, western blotting were the main methods used in the experiment. Our results showed that hydroxysafflor yellow A reduced pancreatic β-cells apoptosis by attenuating oxidative damage, and JNK/c-Jun signaling pathway was involved. It indicated a significant mechanism for the positive impacts of HSYA on oxidative stress induced by high glucose, and provide important basis for using HSYA in diabetic prevention and therapy.


greenmedinfo--2020-12-16--Co-delivery of deferoxamine and hydroxysafflor yellow A to accelerate diabetic wound healing via enh

Co-delivery of deferoxamine and hydroxysafflor yellow A to accelerate diabetic wound healing via enhanced angiogenesis.

Nonhealing chronic wounds on foot induced by diabetes is a complicated pathologic process .
They are mainly caused by impaired neovascularization , neuropathy , and excessive inflammation .
A strategy , which can accelerate the vessel network formation as well as inhibit inflammatory response at the same time , makes it possible for effective diabetic ulcers treatment .
Co-delivery of multiple drugs with complementary bioactivity offers a strategy to properly treat diabetic wound .
We previously demonstrated that hydroxysafflor yellow A ( HSYA ) could accelerate diabetic wound healing through promoting angiogenesis and reducing inflammatory response .
In order to @ @ @ @ @ @ @ pro-angiogenic molecular called deferoxamine ( DFO ) was topically co-administrated with HSYA .
The in vitro results showed that the combination of DFO and HSYA exerted synergistic effect on enhancing angiogenesis by upregulation of hypoxia inducible factor-1 alpha ( HIF-1α ) expression .
The interpenetrating polymer networks hydrogels , characterized by good breathability and water absorption , were designed for co-loading of DFO and HSYA aiming to recruit angiogenesis relative cells and upgrade wound healing in vivo .
Both DFO and HSYA in hydrogel have achieved sustained release .
The in vivo studies @ @ @ @ @ @ @ wound healing .
With a high expression of Hif-1α which is similar to that of normal tissue .
The noninvasive US/PA imaging revealed that the wound could be recovered completely with abundant blood perfusion indermis after given HSYA/DFO hydrogel for 28 days .
In conclusion , combination of pro-angiogenic small molecule DFO and HSYA in hydrogel provides a promising strategy to productively promote diabetic wound healing as well as better the repair quality .

Nonhealing chronic wounds on foot induced by diabetes is a complicated pathologic process. They are mainly caused by impaired neovascularization, neuropathy, and excessive inflammation. A strategy, which can accelerate the vessel network formation as well as inhibit inflammatory response at the same time, makes it possible for effective diabetic ulcers treatment. Co-delivery of multiple drugs with complementary bioactivity offers a strategy to properly treat diabetic wound. We previously demonstrated that hydroxysafflor yellow A (HSYA) could accelerate diabetic wound healing through promoting angiogenesis and reducing inflammatory response. In order to further enhance blood vessel formation, a pro-angiogenic molecular called deferoxamine (DFO) was topically co-administrated with HSYA. The in vitro results showed that the combination of DFO and HSYA exerted synergistic effect on enhancing angiogenesis by upregulation of hypoxia inducible factor-1 alpha (HIF-1α) expression. The interpenetrating polymer networks hydrogels, characterized by good breathability and water absorption, were designed for co-loading of DFO and HSYA aiming to recruit angiogenesis relative cells and upgrade wound healing in vivo. Both DFO and HSYA in hydrogel have achieved sustained release. The in vivo studies indicated that HSYA/DFO hydrogel could accelerate diabetic wound healing. With a high expression of Hif-1α which is similar to that of normal tissue. The noninvasive US/PA imaging revealed that the wound could be recovered completely with abundant blood perfusion indermis after given HSYA/DFO hydrogel for 28 days. In conclusion, combination of pro-angiogenic small molecule DFO and HSYA in hydrogel provides a promising strategy to productively promote diabetic wound healing as well as better the repair quality.


greenmedinfo--2020-12-16--Hydroxysafflor yellow A: A promising therapeutic agent for a broad spectrum of diseases.

Hydroxysafflor yellow A ( HSYA ) is one of the major bioactive and water-soluble compounds isolated from Carthami Flos , the flower of safflower ( L. ) .
As a natural pigment with favorable medical use , HSYA has gained extensive attention due to broad and effective pharmacological activities since first isolation in 1993 .
In clinic , the safflor yellow injection which mainly contains about 80 % HSYA was approved by the China State Food and Drug Administration and used to treat cardiac diseases such as angina pectoris .
In basic pharmacology , HSYA has been proved to exhibit @ @ @ @ @ @ @ include , but not limited to , cardiovascular effect , neuroprotection , liver and lung protection , antitumor activity , metabolism regulation , and endothelium cell protection .
Although a great number of studies have been carried out to prove the pharmacological effects and corresponding mechanisms of HYSA , a systemic review of HYSA has not yet been seen .
Here , we provide a comprehensive summarization of the pharmacological effects of HYSA .
Together with special attention to mechanisms of actions , this review can serve as the basis for further researches @ @ @ @ @ @ @

Hydroxysafflor yellow A (HSYA) is one of the major bioactive and water-soluble compounds isolated from Carthami Flos, the flower of safflower (L.). As a natural pigment with favorable medical use, HSYA has gained extensive attention due to broad and effective pharmacological activities since first isolation in 1993. In clinic, the safflor yellow injection which mainly contains about 80% HSYA was approved by the China State Food and Drug Administration and used to treat cardiac diseases such as angina pectoris. In basic pharmacology, HSYA has been proved to exhibit a broad spectrum of biological effects that include, but not limited to, cardiovascular effect, neuroprotection, liver and lung protection, antitumor activity, metabolism regulation, and endothelium cell protection. Although a great number of studies have been carried out to prove the pharmacological effects and corresponding mechanisms of HYSA, a systemic review of HYSA has not yet been seen. Here, we provide a comprehensive summarization of the pharmacological effects of HYSA. Together with special attention to mechanisms of actions, this review can serve as the basis for further researches and developments of this medicinal compound.


greenmedinfo--2020-12-16--Hydroxysafflor yellow A improves learning and memory in cerebral ischemia reperfusion-injured.

Hydroxysafflor yellow A ( HSYA ) is the major active chemical component of the safflower plant flower , which is widely used in Chinese medicine for cerebrovascular and cardiovascular disease treatment .
Recent studies have demonstrated that HSYA exerts neuroprotective effect on cerebral ischemia , such as neuronal anti-apoptosis , antioxidant activity and oxygen free radical-scavenging .
However , whether and how HSYA has a protective effect on cognitive impairment induced by cerebral ischemia reperfusion remains elusive .
In the present study , by using the middle cerebral artery occlusion ( MCAO ) model , we found that 8 mg/kg @ @ @ @ @ @ @ carotid artery ( CCA ) injection improved impaired cognitive function in Morris water maze ( MWM ) and passive avoidance tasks , but not 4 mg/kg HSYA treatment , suggesting that HSYA treatment in a certain concentration can improve cognitive impairment in MCAO rats .
Furthermore , we found that 8 mg/kg HSYA treatment rescued the impaired long-term potentiation ( LTP ) in hippocampus of MCAO rats .
Taken together , these results for the first time demonstrate that HSYA has the capacity to protect cognitive function and synaptic plasticity against cerebral ischemia-reperfusion @ @ @ @ @ @ @ that HSYA may be a promising alternative for recovery of cognitive dysfunction after brain ischemic injury .

Hydroxysafflor yellow A (HSYA) is the major active chemical component of the safflower plant flower, which is widely used in Chinese medicine for cerebrovascular and cardiovascular disease treatment. Recent studies have demonstrated that HSYA exerts neuroprotective effect on cerebral ischemia, such as neuronal anti-apoptosis, antioxidant activity and oxygen free radical-scavenging. However, whether and how HSYA has a protective effect on cognitive impairment induced by cerebral ischemia reperfusion remains elusive. In the present study, by using the middle cerebral artery occlusion (MCAO) model, we found that 8 mg/kg and 16 mg/kg HSYA administration by common carotid artery (CCA) injection improved impaired cognitive function in Morris water maze (MWM) and passive avoidance tasks, but not 4 mg/kg HSYA treatment, suggesting that HSYA treatment in a certain concentration can improve cognitive impairment in MCAO rats. Furthermore, we found that 8 mg/kg HSYA treatment rescued the impaired long-term potentiation (LTP) in hippocampus of MCAO rats. Taken together, these results for the first time demonstrate that HSYA has the capacity to protect cognitive function and synaptic plasticity against cerebral ischemia-reperfusion injury, and provide a new insight that HSYA may be a promising alternative for recovery of cognitive dysfunction after brain ischemic injury.


greenmedinfo--2020-12-16--Hydroxysafflor yellow A shows protection against PPAR γ inactivation in nitrosative neurons.

Peroxynitrite-mediated nitrosative stress in the brain has been associated with various neurodegenerative disorders .
Recent evidence highlights peroxisome proliferator-activated receptor ( PPAR ) as a critical neuroprotective factor in neurodegenerative diseases .
Here , we observed the effect of the herb hydroxysafflor yellow A ( HSYA ) during nitrosative stress in neurons and investigated the mechanism based on PPARprotection .
We found that a single exposure of primary neurons to peroxynitrite donor SIN-1 caused neuronal injury , which was accompanied by the increase of PPARnitration status and lack of activation of the receptor , as measured by PPARDNA-binding activity , @ @ @ @ @ @ @ stimulation .
The crucial role of PPARin neuronal defense against nitrosative stress was verified by showing that pretreatment with 15d-PGJ2 or rosiglitazone attenuated SIN-1-induced neuronal injury but pretreatment with GW9662 , a PPARantagonist , aggravated SIN-1-induced neuronal injury .
The addition of HSYA not only inhibited SIN-1-induced neuronal damage but prevented PPARnitrative modification and resumed PPARactivity stimulated by either 15d-PGJ2 or rosiglitazone .
Furthermore , HSYA also showed the ability to rescue the neuroprotective effect of 15d-PGJ2 or rosiglitazone when the agonists were coincubated with SIN-1 .
Finally , in vivo experiments demonstrated @ @ @ @ @ @ @ blocked PPARnitration and loss of activity in the SIN-1-injected hippocampus and reversed the increased neuronal susceptibility which was supported by the inhibition of Bcl-2 protein downregulation induced by SIN-1 .
The results suggest that HSYA protects neurons from nitrosative stress through keeping PPARas a functional receptor , allowing a more effective activation of this neuroprotective factor by the endogenous or exogenous agonist .
Our findings provide new clues in understanding the role of the neuroprotective potential of the herbal HSYA .

Peroxynitrite-mediated nitrosative stress in the brain has been associated with various neurodegenerative disorders. Recent evidence highlights peroxisome proliferator-activated receptor(PPAR) as a critical neuroprotective factor in neurodegenerative diseases. Here, we observed the effect of the herb hydroxysafflor yellow A (HSYA) during nitrosative stress in neurons and investigated the mechanism based on PPARprotection. We found that a single exposure of primary neurons to peroxynitrite donor SIN-1 caused neuronal injury, which was accompanied by the increase of PPARnitration status and lack of activation of the receptor, as measured by PPARDNA-binding activity, by agonist (15d-PGJ2 or rosiglitazone) stimulation. The crucial role of PPARin neuronal defense against nitrosative stress was verified by showing that pretreatment with 15d-PGJ2 or rosiglitazone attenuated SIN-1-induced neuronal injury but pretreatment with GW9662, a PPARantagonist, aggravated SIN-1-induced neuronal injury. The addition of HSYA not only inhibited SIN-1-induced neuronal damage but prevented PPARnitrative modification and resumed PPARactivity stimulated by either 15d-PGJ2 or rosiglitazone. Furthermore, HSYA also showed the ability to rescue the neuroprotective effect of 15d-PGJ2 or rosiglitazone when the agonists were coincubated with SIN-1. Finally, in vivo experiments demonstrated that the administration of HSYA also efficiently blocked PPARnitration and loss of activity in the SIN-1-injected hippocampus and reversed the increased neuronal susceptibility which was supported by the inhibition of Bcl-2 protein downregulation induced by SIN-1. The results suggest that HSYA protects neurons from nitrosative stress through keeping PPARas a functional receptor, allowing a more effective activation of this neuroprotective factor by the endogenous or exogenous agonist. Our findings provide new clues in understanding the role of the neuroprotective potential of the herbal HSYA.


greenmedinfo--2020-12-16--Hydroxysafflor yellow A promotes α-synuclein clearance via regulating autophagy in rotenone-induced

Hydroxysafflor yellow A promotes α-synuclein clearance via regulating autophagy in rotenone-induced Parkinson's disease.

Autophagy is an intracellular degradation process that is involved inα-synuclein ( α-syn ) homeostasis and Parkinson 's disease ( PD ) .
The purpose of this study was to investigate whether hydroxysafflor yellow A ( HSYA ) could promote α-syn clearance via regulating autophagy in PD mice .
Male C57BL/6 mice were intraperitoneally treated with HSYA .
Thirty minutes later , they were intragastrically administered with rotenone at a dose of 30 mg/kg .
The hanging wire test was performed at 14 and 28 days .
Then , autophagosomes and ultrastructural changes were examined by transmission electron microscopy .
The @ @ @ @ @ @ @ , α-syn , JNK1 , p-JNK1 , Bcl-2 , p-Bcl-2 , Beclin1 , autophagy-related proteins ( Atg ) 7 and 12-5 , and the LC3-II/LC3-I ratio were investigated by western blot .
The hanging time of HSYA-treated PD mice was significantly increased compared with that of rotenone-induced PD mice ( p < 0.05 or p < 0.01 ) .
Compared with rotenone-induced PD mice , treatment with HSYA augmented the formation of autophagosomes .
The expression of TH , p-JNK1/JNK1 , Beclin1 , Atg7 , Atg12-5 , p-Bcl-2/Bcl-2 , and the LC3-II/LC3-I ratio @ @ @ @ @ @ @ of α-syn was reduced in the rotenone plus HSYA group .
These results indicate that HSYA promoted α-syn clearance via regulating autophagy in rotenone-induced PD mice .

Autophagy is an intracellular degradation process that is involved inα-synuclein (α-syn) homeostasis and Parkinson's disease (PD). The purpose of this study was to investigate whether hydroxysafflor yellow A (HSYA) could promote α-syn clearance via regulating autophagy in PD mice. Male C57BL/6 mice were intraperitoneally treated with HSYA. Thirty minutes later, they were intragastrically administered with rotenone at a dose of 30 mg/kg. The hanging wire test was performed at 14 and 28 days. Then, autophagosomes and ultrastructural changes were examined by transmission electron microscopy. The expression of tyrosine hydroxylase (TH), α-syn, JNK1, p-JNK1, Bcl-2, p-Bcl-2, Beclin1, autophagy-related proteins (Atg) 7 and 12-5, and the LC3-II/LC3-I ratio were investigated by western blot. The hanging time of HSYA-treated PD mice was significantly increased compared with that of rotenone-induced PD mice (p<0.05 or p<0.01). Compared with rotenone-induced PD mice, treatment with HSYA augmented the formation of autophagosomes. The expression of TH, p-JNK1/JNK1, Beclin1, Atg7, Atg12-5, p-Bcl-2/Bcl-2, and the LC3-II/LC3-I ratio were significantly increased, whereas the expression of α-syn was reduced in the rotenone plus HSYA group. These results indicate that HSYA promoted α-syn clearance via regulating autophagy in rotenone-induced PD mice.


greenmedinfo--2020-12-16--Hydroxysafflor yellow A could alleviate inflammatory cell infiltration and other pathological change

Hydroxysafflor yellow A could alleviate inflammatory cell infiltration and other pathological changes in the lungs of chronic obstructive pulmonary disease.

OBJECTIVE : To investigate the attenuating effect of Hydroxysafflor yellow A ( HSYA ) on inflammatory injury in chronic obstructive pulmonary disease ( COPD ) .
METHODS : Rats were randomly assigned to 7 groups according to body weight including normal control group , HSYA blank group ( 76.8 mg/kg ) , COPD group , COPD+HSYA ( 30 , 48 , 76.8 mg/kg ) groups and COPD+dexamethasone ( 2 mg/kg ) , 10 in each group .
Passive cigarette smoke and intratracheal instillation of lipopolysaccharides were used to establish a COPD model in rats .
Hematoxylin and eosin staining of @ @ @ @ @ @ @ polymerase chain reaction ( PCR ) was used to assay mRNA levels of some cytokines in lung tissues , the cytokines in bronchoalveolar lavage fluid ( BALF ) were measured by enzyme-linked immunosorbent assay ( ELISA ) , Western blot analysis was used to determine phosphorylated p38 mitogen-activated protein kinase ( MAPK ) levels in lung tissues , and nuclear factor-κB ( NF-κB ) p65 protein levels in lung tissues were detected by immunohistochemistry .
RESULTS : Lung alveolar septa destruction , alveolus fusion , inflammatory cell infiltration , and bronchiole exudation were @ @ @ @ @ @ @ in the COPD+HSYA group .
The mRNA expression of inflammatory factors were significantly increased in lung tissues from COPD rats ( all P < 0.01 ) and were inhibited by HSYA .
Levels of inflammatory cytokines in BALF of COPD rats were significantly increased ( all P < 0.01 ) which were inhibited by HSYA ( all P < 0.01 , 48 , 76.8 mg/kg ) .
The levels of p38 MAPK phosphorylation and p65 in lung tissues of COPD rats were significantly increased ( all P < 0.01 ) and were suppressed @ @ @ @ @ @ @ , 48 , 76.8 mg/kg ) .
CONCLUSIONS : HSYA could alleviate inflammatory cell infiltration and other pathological changes in the lungs of COPD rats .
HSYA inhibited inflammatory cytokine expression , and increase phosphorylation of p38 MAPK and NF-κB p65 in the lungs of COPD rats .
The protective mechanism of HSYA to inhibit COPD inflammation might be by attenuating NF-κB and p38MAPK signal transduction .

OBJECTIVE: To investigate the attenuating effect of Hydroxysafflor yellow A (HSYA) on inflammatory injury in chronic obstructive pulmonary disease (COPD).
METHODS: Rats were randomly assigned to 7 groups according to body weight including normal control group, HSYA blank group (76.8 mg/kg), COPD group, COPD+HSYA (30, 48, 76.8 mg/kg) groups and COPD+dexamethasone (2 mg/kg), 10 in each group. Passive cigarette smoke and intratracheal instillation of lipopolysaccharides were used to establish a COPD model in rats. Hematoxylin and eosin staining of lung tissue sections was used, real-time polymerase chain reaction (PCR) was used to assay mRNA levels of some cytokines in lung tissues, the cytokines in bronchoalveolar lavage fluid (BALF) were measured by enzyme-linked immunosorbent assay (ELISA), Western blot analysis was used to determine phosphorylated p38 mitogen-activated protein kinase (MAPK) levels in lung tissues, and nuclear factor-κB (NF-κB) p65 protein levels in lung tissues were detected by immunohistochemistry.
RESULTS: Lung alveolar septa destruction, alveolus fusion, inflammatory cell infiltration, and bronchiole exudation were observed. These pathological changes were alleviated in the COPD+HSYA group. The mRNA expression of inflammatory factors were significantly increased in lung tissues from COPD rats (all P<0.01) and were inhibited by HSYA. Levels of inflammatory cytokines in BALF of COPD rats were significantly increased (all P<0.01) which were inhibited by HSYA (all P<0.01, 48, 76.8 mg/kg). The levels of p38 MAPK phosphorylation and p65 in lung tissues of COPD rats were significantly increased (all P<0.01) and were suppressed by HSYA (all P<0.01, 48, 76.8 mg/kg).
CONCLUSIONS: HSYA could alleviate inflammatory cell infiltration and other pathological changes in the lungs of COPD rats. HSYA inhibited inflammatory cytokine expression, and increase phosphorylation of p38 MAPK and NF-κB p65 in the lungs of COPD rats. The protective mechanism of HSYA to inhibit COPD inflammation might be by attenuating NF-κB and p38MAPK signal transduction.


greenmedinfo--2020-12-16--These findings provided experimental evidences that hydroxysafflor yellow A might be a promising ant

These findings provided experimental evidences that hydroxysafflor yellow A might be a promising anticancer agent for liver cancer.

The antitumor effect of hydroxysafflor yellow A ( HSYA ) , an active ingredient of the herb Carthamus tinctorius L. ( Asteraceae ) ( safflower ) , was investigated in the current work .
Researches of HSYA on vasculogenesis inhibition , along with the related molecular mechanisms , including the expression of MMP-2 , MMP-9 , and p38MAPK ( COX-2 , ATF-2 , p-p38MAPK , and p38MAPK ) signaling pathway in H22 tumor-bearing mice or HepG2 cells were performed .
The animal experiments proved the level of MMP-2 and MMP-9 in H22-transplanted tumor tissue in mice markedly decreased by HSYA @ @ @ @ @ @ @ in vitro confirmed that COX-2 expression was reduced significantly via p38MAPK|ATF-2 signaling pathway .
According to the outcomes , HSYA suppressed p38MAPK phosphorylation in a concentration-dependent manner , while exerting no effect on the total p38MAPK protein expression .
It was also showed that suppression of p38 activation by SB203580 decreased the HepG2 cell viability , proliferation , and migration , wherein HSYA exhibited a similar effect .
Furthermore , Western blot analysis on caspase-3 and cleaved-caspase-3 revealed that HSYA could induce apoptosis of HepG2 cells .
These findings provided experimental evidences that @ @ @ @ @ @ @ for HCC .

The antitumor effect of hydroxysafflor yellow A (HSYA), an active ingredient of the herb Carthamus tinctorius L. (Asteraceae) (safflower), was investigated in the current work. Researches of HSYA on vasculogenesis inhibition, along with the related molecular mechanisms, including the expression of MMP-2, MMP-9, and p38MAPK (COX-2, ATF-2, p-p38MAPK, and p38MAPK) signaling pathway in H22 tumor-bearing mice or HepG2 cells were performed. The animal experiments proved the level of MMP-2 and MMP-9 in H22-transplanted tumor tissue in mice markedly decreased by HSYA, and results both in vivo and in vitro confirmed that COX-2 expression was reduced significantly via p38MAPK|ATF-2 signaling pathway. According to the outcomes, HSYA suppressed p38MAPK phosphorylation in a concentration-dependent manner, while exerting no effect on the total p38MAPK protein expression. It was also showed that suppression of p38 activation by SB203580 decreased the HepG2 cell viability, proliferation, and migration, wherein HSYA exhibited a similar effect. Furthermore, Western blot analysis on caspase-3 and cleaved-caspase-3 revealed that HSYA could induce apoptosis of HepG2 cells. These findings provided experimental evidences that HSYA might be a promising anticancer agent for HCC.


greenmedinfo--2020-12-16--Neuroprotection of hydroxysafflor yellow A in experimental cerebral ischemia/reperfusion injury.

Stroke is the second most frequent cause of mortality , resulting in a huge societal burden worldwide .
Timely reperfusion is the most effective therapy ; however , it is difficult to prevent ischemia/reperfusion ( I/R ) injury .
In traditional Chinese medicine , hydroxysafflor yellow A ( HSYA ) has been widely used for the treatment of cerebrovascular disease and as a protective therapy against I/R injury .
Evidence has demonstrated that HSYA could reduce the levels of reactive oxygen species and suppress cellular apoptosis ; however , whether HSYA alters the metabolic profile as its underlying mechanism for @ @ @ @ @ @ @ study , using a metabolomic screening , phenylalanine was identified to significantly increase in an experimental model of mouse cerebral I/R injury .
Notably , western blotting and qPCR analysis were conducted to test the expression level of apoptosis‑associated factors , and HSYA was identified to be able to protect neuronal cells by reducing phenylalanine level associated with I/R injury .
Additionally , these findings were confirmed in primary mouse neurons and PC12 cells exposed to oxygen and glucose deprivation/reoxygenation ( OGD/R ) stress.Of note , HSYA was observed to regulate the mRNA @ @ @ @ @ @ @ hydroxylase , tyrosine aminotransferase and aspartate aminotransferase , which are responsible for phenylalanine metabolism .
Furthermore , by performing mitochondrial labeling and JC‑1 fluorescence assay , HSYA was identified to promote mitochondrial function and biogenesis suppressed by OGD/R .
The findings of the present study demonstrated that I/R injury could increase the levels of phenylalanine , and HSYA may inhibit phenylalanine synthesis to enhance mitochondrial function and biogenesis for neuroprotection .
The present study proposed a novel metabolite biomarker for cerebral I/R injury and the evaluated the efficacy of HSYA as a potential @ @ @ @ @

Stroke is the second most frequent cause of mortality, resulting in a huge societal burden worldwide. Timely reperfusion is the most effective therapy; however, it is difficult to prevent ischemia/reperfusion (I/R) injury. In traditional Chinese medicine, hydroxysafflor yellow A (HSYA) has been widely used for the treatment of cerebrovascular disease and as a protective therapy against I/R injury. Evidence has demonstrated that HSYA could reduce the levels of reactive oxygen species and suppress cellular apoptosis; however, whether HSYA alters the metabolic profile as its underlying mechanism for neuroprotection remains unknown. In the present study, using a metabolomic screening, phenylalanine was identified to significantly increase in an experimental model of mouse cerebral I/R injury. Notably, western blotting and qPCR analysis were conducted to test the expression level of apoptosis‑associated factors, and HSYA was identified to be able to protect neuronal cells by reducing phenylalanine level associated with I/R injury. Additionally, these findings were confirmed in primary mouse neurons and PC12 cells exposed to oxygen and glucose deprivation/reoxygenation (OGD/R) stress.Of note, HSYA was observed to regulate the mRNA expression of key metabolic enzymes, phenylalanine hydroxylase, tyrosine aminotransferase and aspartate aminotransferase, which are responsible for phenylalanine metabolism. Furthermore, by performing mitochondrial labeling and JC‑1 fluorescence assay, HSYA was identified to promote mitochondrial function and biogenesis suppressed by OGD/R. The findings of the present study demonstrated that I/R injury could increase the levels of phenylalanine, and HSYA may inhibit phenylalanine synthesis to enhance mitochondrial function and biogenesis for neuroprotection. The present study proposed a novel metabolite biomarker for cerebral I/R injury and the evaluated the efficacy of HSYA as a potential therapeutic treatment I/R injury.


greenmedinfo--2020-12-16--Hydroxysafflor yellow A (HSYA) alleviates apoptosis and autophagy of neural stem cells induced by he

Hydroxysafflor yellow A (HSYA) alleviates apoptosis and autophagy of neural stem cells induced by heat stress.

This study aimed to explore mechanisms of the effects of hydroxysafflor yellow A ( HSYA ) on neural stem cells @ @ @ @ @ stress ( HS ) .
Rat NSCs cells were cultured at 42 °C to impose @ @ @ @ @ kit-8 and Edu assay were used to analyze NSC proliferation .
Annexin V/PI apoptosis kit @ @ @ @ @ apoptosis .
Expression and phosphorylation of autophagy and apoptosis-associated proteins were determined by western blotting @ @ @ @ @ promoted proliferation and attenuated apoptosis of NSCs after heat stress .
HSYA also increased Bcl-2 @ @ @ @ @ of Bax and cleaved caspase-3 in NSCs induced by heat stress .
In addition , @ @ @ @ @ phosphorylation and MK-2 expression after heat stress , which was consistent with NSCs treated with @ @ @ @ @ .
Furthermore , we demonstrated that heat stress increased LC3-II expression and mTOR phosphorylation , @ @ @ @ @ p62 in NSCs , while HSYA , SB203850 treatment or p38 knockdown reversed these alterations @ @ @ @ @ significantly reversed the apoptosis and autophagy of NSCs induced by heat stress ( P

This study aimed to explore mechanisms of the effects of hydroxysafflor yellow A (HSYA) on neural stem cells (NSCs) after heat stress (HS). Rat NSCs cells were cultured at 42 °C to impose heat stress. Cell counting kit-8 and Edu assay were used to analyze NSC proliferation. Annexin V/PI apoptosis kit was used to detect NSC apoptosis. Expression and phosphorylation of autophagy and apoptosis-associated proteins were determined by western blotting. We showed that HSYAsignificantly promoted proliferation and attenuated apoptosis of NSCs after heat stress. HSYA also increased Bcl-2 expression but decreased the expression of Bax and cleaved caspase-3 in NSCs induced by heat stress. In addition, HSYA decreased p38 and Hsp27-78 phosphorylation and MK-2 expression after heat stress, which was consistent with NSCs treated with SB203850 treatment or p38 knockdown. Furthermore, we demonstrated that heat stress increased LC3-II expression and mTOR phosphorylation, and decreased the expression of p62 in NSCs, while HSYA, SB203850 treatment or p38 knockdown reversed these alterations. In conclusion, HSYA significantly reversed the apoptosis and autophagy of NSCs induced by heat stress (P < 0.05), via downregulating MK2 expression and p38 and Hsp27-78 phosphorylation.


greenmedinfo--2020-12-16--Hydroxysafflor yellow A alleviates ovalbumin-induced asthma.

Hydroxysafflor yellow A ( HSYA ) is an effective ingredient of the Chinese herbL .
In this study , we aimed to evaluate the effects of HSYA on ovalbumin ( OVA ) -induced asthma in guinea pigs , and to elucidate the underlying mechanisms .
We established a guinea pig asthma model by intraperitoneal injection and atomized administration OVA .
Guinea pigs were injected intraperitoneally with HSYA ( 50 , 75 , 112.5 mg/kg ) once daily from days 2 to 22 before OVA administration .
We examined biomarkers including lung function , pulmonary histopathology , immunoglobulin E ( IgE @ @ @ @ @ @ @ and related pathways .
Pathological changes in lung tissues were detected by hematoxylin and eosin and periodic acid-Schiff staining .
Phosphorylation levels of JNK mitogen-activated protein kinase ( MAPK ) , p38 MAPK , ERK MAPK , and inhibitor of nuclear factorκBα ( IκBα ) were detected by western blot .
plasma levels of total IgE , platelet-activating factor ( PAF ) , and interleukin ( IL ) -3 were detected by enzyme-linked immunosorbent assay ( ELISA ) .
Expression levels of tumor necrosis factor ( TNF ) -α , IL-1β , IL-2 @ @ @ @ @ @ @ IL-13 , and interferon ( IFN ) -γ were detected by ELISA and real-time quantitative polymerase chain reaction .
HSYA significantly reduced airway resistance , improved dynamic lung compliance , and attenuated the pathologic changes .
HSYA also inhibited the phosphorylation of JNK MAPK , p38 MAPK , ERK MAPK , and IκBα , and inhibited the OVA-induced elevations of IgE , PAF , IL-1β , IL-6 , IL-4 , IL-5 , and IL-13 and the decreases in TNF-α , IFN-γ , IL-2 , and IL-3 .
These findings suggest that HSYA has @ @ @ @ @ @ @ inhibiting the Th1/Th2 cell imbalance and inhibiting activation of the MAPK signaling pathway .

Hydroxysafflor yellow A (HSYA) is an effective ingredient of the Chinese herbL. In this study, we aimed to evaluate the effects of HSYA on ovalbumin (OVA)-induced asthma in guinea pigs, and to elucidate the underlying mechanisms. We established a guinea pig asthma model by intraperitoneal injection and atomized administration OVA. Guinea pigs were injected intraperitoneally with HSYA (50, 75, 112.5 mg/kg) once daily from days 2 to 22 before OVA administration. We examined biomarkers including lung function, pulmonary histopathology, immunoglobulin E (IgE), Th1/Th2 relative inflammatory mediators, and related pathways. Pathological changes in lung tissues were detected by hematoxylin and eosin and periodic acid-Schiff staining. Phosphorylation levels of JNK mitogen-activated protein kinase (MAPK), p38 MAPK, ERK MAPK, and inhibitor of nuclear factorκBα (IκBα) were detected by western blot. plasma levels of total IgE, platelet-activating factor (PAF), and interleukin (IL)-3 were detected by enzyme-linked immunosorbent assay (ELISA). Expression levels of tumor necrosis factor (TNF)-α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-13, and interferon (IFN)-γ were detected by ELISA and real-time quantitative polymerase chain reaction. HSYA significantly reduced airway resistance, improved dynamic lung compliance, and attenuated the pathologic changes. HSYA also inhibited the phosphorylation of JNK MAPK, p38 MAPK, ERK MAPK, and IκBα, and inhibited the OVA-induced elevations of IgE, PAF, IL-1β, IL-6, IL-4, IL-5, and IL-13 and the decreases in TNF-α, IFN-γ, IL-2, and IL-3. These findings suggest that HSYA has a protective effect on OVA-induced asthma through inhibiting the Th1/Th2 cell imbalance and inhibiting activation of the MAPK signaling pathway.


greenmedinfo--2020-12-16--Hydroxysafflor yellow A may be a potential candidate to treat inflammation-mediated non-small cell l

Hydroxysafflor yellow A may be a potential candidate to treat inflammation-mediated non-small cell lung cancer.

BACKGROUND : Chronic inflammation plays a significant role in the occurrence and development of non-small cell lung cancer ( NSCLC ) .
Hydroxysafflor yellow A ( HSYA ) , a chemical compound of the yellow color pigments extracted from the safflower , has been widely used in clinical treatment with positive antioxidation , anti-inflammation , and antitumor effects .
However , the role and underlying mechanisms of HYSA on development and progress in inflammation-mediated NSCLC are unknown .
METHODS : Cell counting kit-8 , colony formation , EdU , cell apoptosis , wound healing , Transwell migration and invasion , @ @ @ @ @ @ @ ; and Western blotting were conducted using human NSCLC cell lines A549 and H1299 .
RESULTS : Lipopolysaccharide ( LPS ) significantly promoted the proliferation and enhanced colony formation of A549 and H1299 cells , while HYSA notably reversed the effects of LPS .
HYSA induced apoptosis of LPS-mediated A549 and H1299 cells in a dose dependent manner ; and remarkably suppressed migration , invasion , and epithelial-mesenchymal transition ( EMT ) , significantly regulated production of LPS-induced inflammation cytokines , and downregulated protein expression of PI3K/Akt/mTOR and ERK/MAPK signaling pathways in LPS-induced @ @ @ @ @ @ @ PI3K ( LY294002 ) and ERK ( SCH772984 ) inhibitors remarkably inhibited proliferation , migration , invasion , and EMT , and induced apoptosis in LPS-mediated A549 and H1299 cells .
These effects were even more obvious in the presence of HYSA and LY294002 or SCH772984 compared to those of either agent alone .
CONCLUSION : HYSA suppressed LPS-mediated proliferation , migration , invasion , and EMT in A549 and H1299 cells by inhibiting the PI3K/Akt/mTOR and ERK/MAPK signaling pathways , indicating that HYSA may be a potential candidate to treat inflammation-mediated NSCLC @

BACKGROUND: Chronic inflammation plays a significant role in the occurrence and development of non-small cell lung cancer (NSCLC). Hydroxysafflor yellow A (HSYA), a chemical compound of the yellow color pigments extracted from the safflower, has been widely used in clinical treatment with positive antioxidation, anti-inflammation, and antitumor effects. However, the role and underlying mechanisms of HYSA on development and progress in inflammation-mediated NSCLC are unknown.
METHODS: Cell counting kit-8, colony formation, EdU, cell apoptosis, wound healing, Transwell migration and invasion, and enzyme-linked immunosorbent assays; flow cytometry; and Western blotting were conducted using human NSCLC cell lines A549 and H1299.
RESULTS: Lipopolysaccharide (LPS) significantly promoted the proliferation and enhanced colony formation of A549 and H1299 cells, while HYSA notably reversed the effects of LPS. HYSA induced apoptosis of LPS-mediated A549 and H1299 cells in a dose dependent manner; and remarkably suppressed migration, invasion, and epithelial-mesenchymal transition (EMT), significantly regulated production of LPS-induced inflammation cytokines, and downregulated protein expression of PI3K/Akt/mTOR and ERK/MAPK signaling pathways in LPS-induced A549 and H1299 cells. Furthermore, PI3K (LY294002) and ERK (SCH772984) inhibitors remarkably inhibited proliferation, migration, invasion, and EMT, and induced apoptosis in LPS-mediated A549 and H1299 cells. These effects were even more obvious in the presence of HYSA and LY294002 or SCH772984 compared to those of either agent alone.
CONCLUSION: HYSA suppressed LPS-mediated proliferation, migration, invasion, and EMT in A549 and H1299 cells by inhibiting the PI3K/Akt/mTOR and ERK/MAPK signaling pathways, indicating that HYSA may be a potential candidate to treat inflammation-mediated NSCLC.


greenmedinfo--2020-12-16--Inhibitory effect of hydroxysafflor yellow B on the proliferation of human breast cancer MCF-7 cells

Inhibitory effect of hydroxysafflor yellow B on the proliferation of human breast cancer MCF-7 cells.

BACKGROUND : A recent patent has been issued for hydroxysafflor yellow A ( HSYA ) as a drug to prevent blood circulation disorders .
Hydroxysafflor yellow B ( HSYB ) , an isomer of HSYA with antioxidative effects , has been isolated from the florets of Carthamus tinctorius .
The effects of HSYB on the proliferation of cancer cells and its mechanism of action have not been investigated .
OBJECTIVE : The aims of this study were to investigate the anti-cancer effects and the molecular mechanism of HSYB for breast cancer MCF-7 cells .
METHODS : MTT assays and colony @ @ @ @ @ @ @ survival and proliferation of MCF-7 cells , respectively .
Hoechst 33258 and flow cytometry were used to measure cell apoptosis and flow cytometry to determine effects on the cell cycle .
Western blots were used to measure protein levels .
RESULTS : Treatment with HSYB reduced survival and proliferation of human breast cancer MCF-7 cells in a dose-dependent manner .
Furthermore , HSYB arrested the MCF-7 cell cycle at the S phase and downregulated cyclin D1 , cyclin E , and CDK2 .
Compared with a control group , HSYB suppressed the protein @ @ @ @ @ @ @ , and p-AKT in MCF-7 cells .
In addition , HSYB decreased the levels of Bcl- 2 , increased the levels of Bax , cleaved caspase-3 and caspase-9 , and subsequently induced MCF-7 cell apoptosis .
CONCLUSION : These data demonstrate that HSYB arrests the MCF-7 cell cycle at the S phase and induces cell apoptosis .
Patent US20170246228 indicates that HSYB can be potentially used for the prevention and treatment of human breast cancer .

BACKGROUND: A recent patent has been issued for hydroxysafflor yellow A (HSYA) as a drug to prevent blood circulation disorders. Hydroxysafflor yellow B (HSYB), an isomer of HSYA with antioxidative effects, has been isolated from the florets of Carthamus tinctorius. The effects of HSYB on the proliferation of cancer cells and its mechanism of action have not been investigated.
OBJECTIVE: The aims of this study were to investigate the anti-cancer effects and the molecular mechanism of HSYB for breast cancer MCF-7 cells.
METHODS: MTT assays and colony formation assays were used to assess the survival and proliferation of MCF-7 cells, respectively. Hoechst 33258 and flow cytometry were used to measure cell apoptosis and flow cytometry to determine effects on the cell cycle. Western blots were used to measure protein levels.
RESULTS: Treatment with HSYB reduced survival and proliferation of human breast cancer MCF-7 cells in a dose-dependent manner. Furthermore, HSYB arrested the MCF-7 cell cycle at the S phase and downregulated cyclin D1, cyclin E, and CDK2. Compared with a control group, HSYB suppressed the protein levels of p-PI3K, PI3K, AKT, and p-AKT in MCF-7 cells. In addition, HSYB decreased the levels of Bcl- 2, increased the levels of Bax, cleaved caspase-3 and caspase-9, and subsequently induced MCF-7 cell apoptosis.
CONCLUSION: These data demonstrate that HSYB arrests the MCF-7 cell cycle at the S phase and induces cell apoptosis. Patent US20170246228 indicates that HSYB can be potentially used for the prevention and treatment of human breast cancer.


greenmedinfo--2020-12-17--Hydroxysafflor yellow A attenuates the apoptosis of peripheral blood CD4 + T lymphocytes in a murine

Hydroxysafflor yellow A attenuates the apoptosis of peripheral blood CD4 + T lymphocytes in a murine model of sepsis.

Sepsis is generally considered as a severe condition of inflammation that leads to lymphocyte apoptosis and multiple organ dysfunction .
Hydroxysafflor yellow A ( HSYA ) exerts anti-inflammatory and anti-apoptotic effects in infectious diseases .
However , the therapeutic effect of HSYA on polymicrobial sepsis remains unknown .
This study was undertaken to investigate the therapeutic effects and the mechanisms of action of HSYA on immunosuppression in a murine model of sepsis induced by cecal ligation and puncture ( CLP ) .
NIH mice were randomly divided into four groups : control group , sham group , CLP group , @ @ @ @ @ @ @ mg/kg ) was intravenously injected into experimental mice at 12 h before CLP , concurrent with CLP and 12 h after CLP .
The levels of circulating inflammatory cytokines , the apoptosis of CD4and CD8T lymphocytes , and protein expression of cytochrome C ( Cytc ) , Bax , Bcl-2 , cleaved caspase-9 , and cleaved caspase-3 were examined .
Plasma levels of IL-6 , IL-10 and TNF-alpha as well as the apoptosis of CD4T lymphocytes were increased compared with sham group .
These changes were accompanied by increases of pro-apoptotic proteins including @ @ @ @ @ @ @ and cleaved caspase-3 and decreases of anti-apoptotic protein Bcl-2 in CD4T lymphocytes from mice undergoing CLP .
In contrast , we fail to observe significant effect of HSYA on the apoptosis of CD8T lymphocytes in CLP-treated group .
Of note , HSYA treatment reversed all above changes observed in CD4T lymphocytes , and significantly increased the ratio of CD4 : CD8T lymphocytes in CLP-treated mice .
In conclusion , HSYA was an effective therapeutic agent in ameliorating sepsis-induced apoptosis of CD4T lymphocytes probably through its anti-inflammatory and anti-apoptotic effects .

Sepsis is generally considered as a severe condition of inflammation that leads to lymphocyte apoptosis and multiple organ dysfunction. Hydroxysafflor yellow A (HSYA) exerts anti-inflammatory and anti-apoptotic effects in infectious diseases. However, the therapeutic effect of HSYA on polymicrobial sepsis remains unknown. This study was undertaken to investigate the therapeutic effects and the mechanisms of action of HSYA on immunosuppression in a murine model of sepsis induced by cecal ligation and puncture (CLP). NIH mice were randomly divided into four groups: control group, sham group, CLP group, and CLP+HSYA group. HSYA (120 mg/kg) was intravenously injected into experimental mice at 12 h before CLP, concurrent with CLP and 12 h after CLP. The levels of circulating inflammatory cytokines, the apoptosis of CD4and CD8T lymphocytes, and protein expression of cytochrome C (Cytc), Bax, Bcl-2, cleaved caspase-9, and cleaved caspase-3 were examined. Plasma levels of IL-6, IL-10 and TNF-alpha as well as the apoptosis of CD4T lymphocytes were increased compared with sham group. These changes were accompanied by increases of pro-apoptotic proteins including Cytc, Bax, cleaved caspase-9, and cleaved caspase-3 and decreases of anti-apoptotic protein Bcl-2 in CD4T lymphocytes from mice undergoing CLP. In contrast, we fail to observe significant effect of HSYA on the apoptosis of CD8T lymphocytes in CLP-treated group. Of note, HSYA treatment reversed all above changes observed in CD4T lymphocytes, and significantly increased the ratio of CD4:CD8T lymphocytes in CLP-treated mice. In conclusion, HSYA was an effective therapeutic agent in ameliorating sepsis-induced apoptosis of CD4T lymphocytes probably through its anti-inflammatory and anti-apoptotic effects.


greenmedinfo--2020-12-16--Seven Tips for Beating Holiday Stress

Seven Tips for Beating Holiday Stress

Running on empty this holiday season ?
Here are the top seven ways to de-stress , beat holiday stress and slide into the New Year feeling your best During the holidays , it 's tempting to go all-out for those you love .
From cooking elaborate meals to shopping for the perfect gifts for friends and family , it 's natural to want to give your best so you can show them they are appreciated at this special time of year .
But remember the oxygen mask theory -- you ca n't help those who depend on you if you @ @ @ @ @ @ @ , it 's more important than ever to fill yourself up first before trying to uplift others .
So while you 're decking the halls and filling your shopping cart to make everyone 's holiday memorable , remember to take time out for yourself .
These seven tips for beating holiday stress can help you remain calm and centered throughout the festive whirlwind .
Get a jump-start on a healthy New Year by resolving to prioritize sleep during the holidays .
Practicing sleep hygiene is important for both physical and mental health .
@ @ @ @ @ @ @ around sleep , you may not be setting yourself up for optimal rejuvenation from time spent in bed .
By implementing a few conscious and consistent nightly habits , you 'll ensure that your down time sets you up for a great tomorrow .
First , make your bed as inviting as possible by replacing your worn-out or unsupportive mattress with one that supports healthy sleep posture .
Be sure to also choose a mattress made from natural materials , without chemicals .
To keep bed clothes fresh between washings , make a @ @ @ @ @ @ @ drops of lavender essential oil ( known for its soothing properties ) to a small spray bottle of filtered water .
Mist sheets and pillowcases when you make your bed in the morning and once again before settling into bed .
The scent of lavender will calm your mind and signal your body that it 's time to relax .
Next , prepare for sleep by instituting a wind-down period one to two hours before bedtime .
Minimize the use of screens and dim overhead lights in favor of task lighting .
Soften @ @ @ @ @ @ @ activity to begin relaxing your body and mind .
If you 're serious about getting good sleep , consider banning all screens , including the television , from your bedroom .
Exposure to unnatural light , especially blue light from screens , can alter your body 's circadian rhythm , your natural , internal synchronization with the sun .
Research has shown that even brief exposures to blue light can lower levels of melatonin secretion , the hormone that helps you feel sleepy at night .
[ i ] By creating and practicing @ @ @ @ @ @ @ to your body that it 's time to relax , recharge and restore .
Getting regular , deep sleep will provide a sustainable foundation for good moods and high energy so you can handle whatever the elves put on your to-do list .
It 's always important to eat clean , nutrient-dense food .
But it takes on even greater significance when colder , dryer weather moves in and the holiday pace creates more demands on your time .
Even though a cookie tray may always be within reach , do n't risk @ @ @ @ @ @ @ food over the holidays .
Many seasonal dishes rely on ingredients like sugar , which , taken in excess , can wreak havoc on your health .
With more opportunities for indulgent dining , it 's important to strike a balance by eating clean , plant-based whole foods for most of your regular meals .
To maintain daily energy levels and ensure that you do n't enter the New Year with too much `` jingle '' in your belly , aim for a minimum of five to seven servings of fruits and vegetables @ @ @ @ @ @ @ vegetables not only provide your body with fiber and energy-boosting carbohydrates , they are a great source of vitamins , minerals and essential phytonutrients that have been associated with reduced risks for heart disease and some cancers .
[ ii ] While you 're busy with your holiday task list , do n't forget to stay hydrated .
Keep a refillable water bottle on-hand and aim for drinking around three to four liters of pure , filtered water each day .
[ iii ] With your year-end focus shifting to what you can @ @ @ @ @ @ @ tempting to forego regular exercise during the holidays .
But this is not the time to slack on self-care .
The hectic pace of the season demands that you consider your own needs , and consistent exercise is key to staying fit , healthy and high-energy into the New Year .
With extra demands on your time creating changes to your normal routine , it 's more important than ever to schedule your workouts .
Resolve to prioritize `` me time '' so that it does n't fall off your calendar .
Enlist @ @ @ @ @ @ @ committed to your workout goals , or , if weather permits , meet up with a neighbor for a brisk daily walk .
While it may seem ambitious to maintain a regular exercise regimen with so much on your plate , the benefits of even low levels of exercise more than justify the calorie expenditure and time spent .
Studies show that burning around 1000 kcal per week , which you can accomplish with around 30 minutes of moderate exercise just three times per week , can reduce all-cause mortality by as much @ @ @ @ @ @ @ The benefits of exercise are n't just physical , they can also help you to better manage the pressure and tension of the holidays .
Routine physical activity is associated with improved mood and reduced feelings of stress , anxiety and depression .
[ v ] What better gift can you give your loved ones than a longer , happier life ?
4 .
Be Kind to Yourself Why is it sometimes easier to show compassion and caring to others than it is to be kind to yourself ?
Social and religious messaging @ @ @ @ @ @ @ of personal development , but compassion rarely flows from a space of feeling depleted .
This holiday , practice filling your spiritual tank by being your own best friend .
Carve out time for yourself each week to `` do nothing '' or to do those things that serve you and you alone .
Reread your favorite novel , or take long , luxurious baths with candles and Epsom salts or magnesium flakes .
As you soak , meditate on the many things you are thankful for this year .
The relaxing effects @ @ @ @ @ @ @ sleep [ vi ] and relieve muscle tension , [ vii ] and the time spent away from noise and distraction can restore a sense of calm during the hectic season .
At this time of giving to others , do n't forget to also be generous with yourself .
Catch negative self-talk and replace it with the same words you would say to a good friend .
By taking a conscious break , even for a few moments , to befriend yourself , you will embody the grace of the season and @ @ @ @ @ @ @ that your well-being matters , too .
5 .
Get Outside the Box While the weather outside may be frightful at times during the holidays , the benefits of spending time outdoors are nothing short of delightful for your health .
While much has been said about the hazards of too much sun exposure , the World Health Organization has reported that a much larger worldwide disease burden results from very low levels of ultraviolet radiation ( UVR ) exposure .
[ viii ] At least 1,000 different genes governing nearly every tissue @ @ @ @ @ @ @ regulated by vitamin D through photosynthesis .
[ ix ] To reduce your risk of various autoimmune and musculoskeletal diseases , as well as to help you de-stress naturally , make a point of getting outside your four walls and spending time outdoors this holiday season .
There are lots of ways to get outside , but consider a few holiday-specific ideas , like taking a stroll through your neighborhood to see the holiday lights or walking through a seasonal display in your town .
Woods and parks are generally less trafficked in @ @ @ @ @ @ @ and hit the trail .
You can even make yard chores festive by clearing away any remaining fall debris and hanging up some holiday decorations .
You 'll not only get a vitamin D boost -- provided you 're in a climate that allows you to expose enough skin to the sunlight even in the winter months -- but you can count these activities as a great way to exercise and boost your holiday spirit all at the same time .
If cold weather prevents you from being able to produce vitamin D @ @ @ @ @ @ @ be necessary , but getting outdoors is highly recommended nonetheless .
With the modern emphasis on commercial gift-giving , it may be easy to forget what this time of year is truly about .
If you feel overwhelmed by expectations and a long to-do list , take a break from the noise and refocus on your personal and family traditions .
Rather than spending time in traffic going to crowded shopping centers or using valuable hours up shopping online , consider unboxing your favorite holiday activities or creating new customs that have meaning @ @ @ @ @ @ @ festive music while baking or watching a time-honored , favorite holiday program can feel like spending time with an old friend .
Connect with elders in your family or community and ask them to tell you stories from holidays ' past .
When bad weather dictates an indoor day , grab the kids , clear the kitchen table and make fun crafts to decorate your home or give as gifts at church , work or school .
By refocusing on your true values instead of what the media says you should be focused @ @ @ @ @ @ @ and connect with the true meaning of the holidays .
Giving presents often takes the form of things wrapped in shiny boxes , but what if you took the time to give your presence this holiday season ?
While it has become commonplace to snap selfies and share activities on social media , try taking a break from digital devices this holiday to focus on simply being with the people and places you love .
Feeling a sense of connection is vital to your mental health and well-being .
Research has shown that @ @ @ @ @ @ @ have lower levels of depression and anxiety , higher self-esteem and a greater sense of empathy and trust .
[ x ] The modern digital era has produced a myriad of ways to connect , but unfortunately our devices often serve to keep us further apart in the ways that truly matter .
Whenever possible , put down your phone and allow yourself to be fully present in moments of connecting with others .
Whether you 're dealing with clients or colleagues at work , engaging with employees in a store or spending @ @ @ @ @ @ @ a point of enriching each person through your connection .
Something as simple as making eye contact and extending a heartfelt `` thank you '' can create a ripple effect of positive energy that deeply impacts someone 's day .
By taking just a moment and applying positive focus to each connection you make , you can embody the spirit of giving with your positivity and good will .
You never know how deeply you may impact someone with a simple act of kindness .
Is n't that what the holidays are truly @ @ @ @ @ @ @ , P. J. , & Willett , W. C. ( 2010 ) .
Essentials of healthy eating : a guide .
Journal of midwifery & women 's health , 55 ( 6 ) , 492-501. https : //doi.org/10.1016/j.jmwh.2010.06.019 [ iv ] Warburton , D. E. , Nicol , C. W. , & Bredin , S. S. ( 2006 ) .
Health benefits of physical activity : the evidence .
CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne , 174 ( 6 ) , 801-809. https : //doi.org/10.1503/cmaj.051351 [ v @ @ @ @ @ @ @ , C. W. , & Bredin , S. S. ( 2006 ) .
Health benefits of physical activity : the evidence .
CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne , 174 ( 6 ) , 801-809. https : //doi.org/10.1503/cmaj.051351 [ vi ] Behnood Abbasi , Masud Kimiagar , Khosro Sadeghniiat , Minoo M Shirazi , Mehdi Hedayati , Bahram Rashidkhani .
The effect of magnesium supplementation on primary insomnia in elderly : A double-blind placebo-controlled clinical trial .
J Res Med Sci .
2012 Dec ; 17 ( @ @ @ @ @ @ @ [ x ] Stanford Medicine , The Center for Compassion and Altruism Research and Education , Connectedness & Health : The Science of Social Connection .
https : //ccare.stanford.edu/uncategorized/connectedness-health-the-science-of-social-connection-infographic/

Visit our Re-post guidelines This article is copyrighted by GreenMedInfo LLC, 2020
Running on empty this holiday season? Here are the top seven ways to de-stress, beat holiday stress and slide into the New Year feeling your best
During the holidays, it's tempting to go all-out for those you love. From cooking elaborate meals to shopping for the perfect gifts for friends and family, it's natural to want to give your best so you can show them they are appreciated at this special time of year.
But remember the oxygen mask theory -- you can't help those who depend on you if you're not breathing easy. This year, it's more important than ever to fill yourself up first before trying to uplift others.
So while you're decking the halls and filling your shopping cart to make everyone's holiday memorable, remember to take time out for yourself. These seven tips for beating holiday stress can help you remain calm and centered throughout the festive whirlwind.
1. Practice Sleep Hygiene
Get a jump-start on a healthy New Year by resolving to prioritize sleep during the holidays. Practicing sleep hygiene is important for both physical and mental health. If you don't have consistent habits around sleep, you may not be setting yourself up for optimal rejuvenation from time spent in bed. By implementing a few conscious and consistent nightly habits, you'll ensure that your down time sets you up for a great tomorrow.
First, make your bed as inviting as possible by replacing your worn-out or unsupportive mattress with one that supports healthy sleep posture. Be sure to also choose a mattress made from natural materials, without chemicals. To keep bed clothes fresh between washings, make a relaxing aromatherapy spray.
Add around 20 drops of lavender essential oil (known for its soothing properties) to a small spray bottle of filtered water. Mist sheets and pillowcases when you make your bed in the morning and once again before settling into bed. The scent of lavender will calm your mind and signal your body that it's time to relax.
Next, prepare for sleep by instituting a wind-down period one to two hours before bedtime. Minimize the use of screens and dim overhead lights in favor of task lighting. Soften the volume of conversations and reduce strenuous activity to begin relaxing your body and mind.
If you're serious about getting good sleep, consider banning all screens, including the television, from your bedroom. Exposure to unnatural light, especially blue light from screens, can alter your body's circadian rhythm, your natural, internal synchronization with the sun. Research has shown that even brief exposures to blue light can lower levels of melatonin secretion, the hormone that helps you feel sleepy at night.[i]
By creating and practicing bedtime rituals, you send a signal to your body that it's time to relax, recharge and restore. Getting regular, deep sleep will provide a sustainable foundation for good moods and high energy so you can handle whatever the elves put on your to-do list.
2. Eat Nutritious Food
It's always important to eat clean, nutrient-dense food. But it takes on even greater significance when colder, dryer weather moves in and the holiday pace creates more demands on your time. Even though a cookie tray may always be within reach, don't risk a dip in well-being by skipping real food over the holidays.
Many seasonal dishes rely on ingredients like sugar, which, taken in excess, can wreak havoc on your health. With more opportunities for indulgent dining, it's important to strike a balance by eating clean, plant-based whole foods for most of your regular meals.
To maintain daily energy levels and ensure that you don't enter the New Year with too much "jingle" in your belly, aim for a minimum of five to seven servings of fruits and vegetables in your daily diet.
Fruits and vegetables not only provide your body with fiber and energy-boosting carbohydrates, they are a great source of vitamins, minerals and essential phytonutrients that have been associated with reduced risks for heart disease and some cancers.[ii] While you're busy with your holiday task list, don't forget to stay hydrated. Keep a refillable water bottle on-hand and aim for drinking around three to four liters of pure, filtered water each day.[iii]
3. Make Time for Exercise
With your year-end focus shifting to what you can do for others, it may be tempting to forego regular exercise during the holidays. But this is not the time to slack on self-care. The hectic pace of the season demands that you consider your own needs, and consistent exercise is key to staying fit, healthy and high-energy into the New Year.
With extra demands on your time creating changes to your normal routine, it's more important than ever to schedule your workouts. Resolve to prioritize "me time" so that it doesn't fall off your calendar. Enlist an exercise buddy to help you stay committed to your workout goals, or, if weather permits, meet up with a neighbor for a brisk daily walk.
While it may seem ambitious to maintain a regular exercise regimen with so much on your plate, the benefits of even low levels of exercise more than justify the calorie expenditure and time spent. Studies show that burning around 1000 kcal per week, which you can accomplish with around 30 minutes of moderate exercise just three times per week, can reduce all-cause mortality by as much as 30%.[iv]
The benefits of exercise aren't just physical, they can also help you to better manage the pressure and tension of the holidays. Routine physical activity is associated with improved mood and reduced feelings of stress, anxiety and depression.[v] What better gift can you give your loved ones than a longer, happier life?
4. Be Kind to Yourself
Why is it sometimes easier to show compassion and caring to others than it is to be kind to yourself? Social and religious messaging can imply that selflessness is the epitome of personal development, but compassion rarely flows from a space of feeling depleted. This holiday, practice filling your spiritual tank by being your own best friend.
Carve out time for yourself each week to "do nothing" or to do those things that serve you and you alone. Reread your favorite novel, or take long, luxurious baths with candles and Epsom salts or magnesium flakes. As you soak, meditate on the many things you are thankful for this year. The relaxing effects of magnesium can improve your quality of sleep[vi] and relieve muscle tension,[vii] and the time spent away from noise and distraction can restore a sense of calm during the hectic season.
At this time of giving to others, don't forget to also be generous with yourself. Catch negative self-talk and replace it with the same words you would say to a good friend. By taking a conscious break, even for a few moments, to befriend yourself, you will embody the grace of the season and send a signal to your unconscious mind that your well-being matters, too.
5. Get Outside the Box
While the weather outside may be frightful at times during the holidays, the benefits of spending time outdoors are nothing short of delightful for your health. While much has been said about the hazards of too much sun exposure, the World Health Organization has reported that a much larger worldwide disease burden results from very low levels of ultraviolet radiation (UVR) exposure.[viii]
At least 1,000 different genes governing nearly every tissue in the body are believed to be regulated by vitamin D 3 through photosynthesis.[ix] To reduce your risk of various autoimmune and musculoskeletal diseases, as well as to help you de-stress naturally, make a point of getting outside your four walls and spending time outdoors this holiday season.
There are lots of ways to get outside, but consider a few holiday-specific ideas, like taking a stroll through your neighborhood to see the holiday lights or walking through a seasonal display in your town. Woods and parks are generally less trafficked in winter months, so grab the dog and hit the trail. You can even make yard chores festive by clearing away any remaining fall debris and hanging up some holiday decorations.
You'll not only get a vitamin D boost -- provided you're in a climate that allows you to expose enough skin to the sunlight even in the winter months --but you can count these activities as a great way to exercise and boost your holiday spirit all at the same time. If cold weather prevents you from being able to produce vitamin D via your skin, a supplement may be necessary, but getting outdoors is highly recommended nonetheless.
6. Focus on Traditions
With the modern emphasis on commercial gift-giving, it may be easy to forget what this time of year is truly about. If you feel overwhelmed by expectations and a long to-do list, take a break from the noise and refocus on your personal and family traditions.
Rather than spending time in traffic going to crowded shopping centers or using valuable hours up shopping online, consider unboxing your favorite holiday activities or creating new customs that have meaning for you and your family. Playing festive music while baking or watching a time-honored, favorite holiday program can feel like spending time with an old friend.
Connect with elders in your family or community and ask them to tell you stories from holidays' past. When bad weather dictates an indoor day, grab the kids, clear the kitchen table and make fun crafts to decorate your home or give as gifts at church, work or school. By refocusing on your true values instead of what the media says you should be focused on, you can center, de-stress and connect with the true meaning of the holidays.
7. Be Present
Giving presents often takes the form of things wrapped in shiny boxes, but what if you took the time to give your presence this holiday season? While it has become commonplace to snap selfies and share activities on social media, try taking a break from digital devices this holiday to focus on simply being with the people and places you love.
Feeling a sense of connection is vital to your mental health and well-being. Research has shown that people who feel more connected to others have lower levels of depression and anxiety, higher self-esteem and a greater sense of empathy and trust.[x] The modern digital era has produced a myriad of ways to connect, but unfortunately our devices often serve to keep us further apart in the ways that truly matter.
Whenever possible, put down your phone and allow yourself to be fully present in moments of connecting with others. Whether you're dealing with clients or colleagues at work, engaging with employees in a store or spending time with friends and family, make a point of enriching each person through your connection. Something as simple as making eye contact and extending a heartfelt "thank you" can create a ripple effect of positive energy that deeply impacts someone's day.
By taking just a moment and applying positive focus to each connection you make, you can embody the spirit of giving with your positivity and good will. You never know how deeply you may impact someone with a simple act of kindness. Isn't that what the holidays are truly all about?
References
[i] Harvard Medical School, Harvard Health Letter, Blue light has a dark side. https://www.health.harvard.edu/staying-healthy/blue-light-has-a-dark-side


greenmedinfo--2020-12-18--Pharmacological potential of the combination of Salvia miltiorrhiza and Carthamus tinctorius for dia

Pharmacological potential of the combination of Salvia miltiorrhiza and Carthamus tinctorius for diabetes mellitus and its cardiovascular complications.

Metabolic syndrome , such as diabetes mellitus , obesity , atherosclerosis , and high blood pressure ( HBP ) , are closely linked pathophysiologically .
However , current monotherapies for metabolic syndrome fail to target the multifactorial pathology via multiple mechanisms , as well as resolving the dysfunctionality of the cells and organs of the body .
We aimed to provide a comprehensive and up-to-date review of the pharmacological advances , therapeutic potential , and phytochemistry of Salvia miltiorrhiza , Carthamus tinctorius , and Danhong injection ( DHI ) .
We discussed the molecular mechanisms of the bioactive constituents relating @ @ @ @ @ @ @ further research and drug development .
Interestingly , Salvia miltiorrhiza , Carthamus tinctorius , and DHI have anti-inflammatory , anti-glycemic , anti-thrombotic , and anti-cancer properties ; and they mainly act by targeting the dysfunctional vasculatures including the inflammatory components of the disease to provide vascular repair as well as resolving oxidative stress .
The major bioactive chemical constituents of these plants include polyphenolic acids , diterpene compounds , carthamin , and hydroxysafflor yellow A .
Treatment of diabetes mellitus and its associated cardiovascular complication requires a comprehensive approach involving the use of @ @ @ @ @ @ @ , Honghua , and DHI target the multiple risk factors regulating the physiologic function of the body and restore normalcy , apart from the traditional advice on exercise and diet control as treatment options in a metabolic syndrome patient .

Metabolic syndrome, such as diabetes mellitus, obesity, atherosclerosis, and high blood pressure (HBP), are closely linked pathophysiologically. However, current monotherapies for metabolic syndrome fail to target the multifactorial pathology via multiple mechanisms, as well as resolving the dysfunctionality of the cells and organs of the body. We aimed to provide a comprehensive and up-to-date review of the pharmacological advances, therapeutic potential, and phytochemistry of Salvia miltiorrhiza, Carthamus tinctorius, and Danhong injection (DHI). We discussed the molecular mechanisms of the bioactive constituents relating to diabetes mellitus and metabolic disease for further research and drug development. Interestingly, Salvia miltiorrhiza, Carthamus tinctorius, and DHI have anti-inflammatory, anti-glycemic, anti-thrombotic, and anti-cancer properties; and they mainly act by targeting the dysfunctional vasculatures including the inflammatory components of the disease to provide vascular repair as well as resolving oxidative stress. The major bioactive chemical constituents of these plants include polyphenolic acids, diterpene compounds, carthamin, and hydroxysafflor yellow A. Treatment of diabetes mellitus and its associated cardiovascular complication requires a comprehensive approach involving the use of appropriate traditional Chinese medicine formula. Danshen, Honghua, and DHI target the multiple risk factors regulating the physiologic function of the body and restore normalcy, apart from the traditional advice on exercise and diet control as treatment options in a metabolic syndrome patient.


greenmedinfo--2020-12-18--Safflower seed extract synergizes the therapeutic effect of cisplatin and reduces cisplatin-induced

Safflower seed extract synergizes the therapeutic effect of cisplatin and reduces cisplatin-induced nephrotoxicity.

Safflower seed is effective against oxidative stress , mediating the activation of the apoptotic signaling pathway in the renal tissues of cisplatin-treated mice .
The anticancer activity of safflower in various cancer cell lines has also been reported .
The present study was conducted to evaluate the potential synergistic anticancer effects of the co-treatment of safflower seed extracts and cisplatin in RKO cells and in BALB/c mice bearing RKO cell-derived human colorectal tumors .
In the cellular system , RKO cells were treated with safflower seed extract in the presence or absence of cisplatin for 48 h and the cytotoxicity @ @ @ @ @ @ @ the in vivo system , mice were injected with RKO cells and subsequently orally administered 100 or 200 mg/kg body weight safflower seed extract plus cisplatin-treated or untreated mice for 3 days to examine the inhibitory effect on the tumor .
Treatment with safflower seed extract or cisplain to RKO cells resulted in a greater cell death than in with untreated cells .
In the RKO cells co-treated with both safflower seed extract and cisplatin , greater cell damage was observed .
In addition , mice co-administered safflower seed extract and cisplatin had @ @ @ @ @ @ @ were indicative of less damage to the kidney , and had a lower solid tumor mass and higher expression of the caspase-3 protein .
The results showed that safflower seed extract was highly toxic to RKO cells and inhibited tumor growth in cisplatin-treated mice through renoprotective effects .

Safflower seed is effective against oxidative stress, mediating the activation of the apoptotic signaling pathway in the renal tissues of cisplatin-treated mice. The anticancer activity of safflower in various cancer cell lines has also been reported. The present study was conducted to evaluate the potential synergistic anticancer effects of the co-treatment of safflower seed extracts and cisplatin in RKO cells and in BALB/c mice bearing RKO cell-derived human colorectal tumors. In the cellular system, RKO cells were treated with safflower seed extract in the presence or absence of cisplatin for 48 h and the cytotoxicity was evaluated by using microscopy. In the in vivo system, mice were injected with RKO cells and subsequently orally administered 100 or 200 mg/kg body weight safflower seed extract plus cisplatin-treated or untreated mice for 3 days to examine the inhibitory effect on the tumor. Treatment with safflower seed extract or cisplain to RKO cells resulted in a greater cell death than in with untreated cells. In the RKO cells co-treated with both safflower seed extract and cisplatin, greater cell damage was observed. In addition, mice co-administered safflower seed extract and cisplatin had lower concentrations of serum creatinine, which were indicative of less damage to the kidney, and had a lower solid tumor mass and higher expression of the caspase-3 protein. The results showed that safflower seed extract was highly toxic to RKO cells and inhibited tumor growth in cisplatin-treated mice through renoprotective effects.


greenmedinfo--2020-12-18--Safflower seed extract and its oil can improve fructose-induced metabolic syndrome.

ETHNOPHARMACOLOGICAL RELEVANCE : Safflower ( Carthamus tinctorius ) has many applications in folk medicine .
Its oil is used traditionally to treat obesity and other metabolic disorders .
The anti-hypercholesterolemic and antioxidant effects of this plant have been well documented , but the anti-inflammatory effects and its role on fatty acid oxidation and homeostasis of trace elements are not fully understood .
OBJECTIVE : The aim of this study was to evaluate the protective effects of different doses of oil and extract of safflower seed against fructose induced metabolic syndrome by investigating the homeostasis of trace elements , TNF-α , @ @ @ @ @ @ @ Eighty adult male Sprague-Dawley rats were randomly divided into ten groups and treated daily for 16 weeks .
At the end of the study , plasma levels of liver enzymes , lipid profiles , blood glucose , insulin and TNF-α were measured .
The levels of antioxidant enzymes and lipid peroxidation were also measured along with the expression of CD36 , fatty acyl-CoA synthetase ( FAS ) , and Carnitine palmitoyl transferase I ( CPT-1 ) beta genes in the liver .
RESULTS : The antioxidant enzymes activity significantly decreased and lipid peroxidation @ @ @ @ @ @ @ and TNF-α significantly increased in fructose-induced metabolic syndrome compared to the control groups , as well as the level of some trace elements significantly changed ( p CONCLUSION : It can be concluded that safflower seed extract and its oil can improve fructose-induced metabolic syndrome through antioxidant and anti-inflammatory effects , adjustment of homeostasis of trace elements , and enhancing the beta-oxidation capacity of the liver by increasing the expression of CD36 , FAS , and CPT-1beta genes .

ETHNOPHARMACOLOGICAL RELEVANCE: Safflower (Carthamus tinctorius) has many applications in folk medicine. Its oil is used traditionally to treat obesity and other metabolic disorders. The anti-hypercholesterolemic and antioxidant effects of this plant have been well documented, but the anti-inflammatory effects and its role on fatty acid oxidation and homeostasis of trace elements are not fully understood.
OBJECTIVE: The aim of this study was to evaluate the protective effects of different doses of oil and extract of safflower seed against fructose induced metabolic syndrome by investigating the homeostasis of trace elements, TNF-α, and fatty acids metabolism.
METHODS: Eighty adult male Sprague-Dawley rats were randomly divided into ten groups and treated daily for 16 weeks. At the end of the study, plasma levels of liver enzymes, lipid profiles, blood glucose, insulin and TNF-α were measured. The levels of antioxidant enzymes and lipid peroxidation were also measured along with the expression of CD36, fatty acyl-CoA synthetase (FAS), and Carnitine palmitoyl transferase I (CPT-1) beta genes in the liver.
RESULTS: The antioxidant enzymes activity significantly decreased and lipid peroxidation, lipid profiles, liver enzymes, and TNF-α significantly increased in fructose-induced metabolic syndrome compared to the control groups, as well as the level of some trace elements significantly changed (p < 0.05). Treatment with oil and safflower seed extract in a dose dependent manner could improve biochemical parameters in groups of metabolic syndrome treated with oil and extract compared to metabolic syndrome (p < 0.05). The results also showed that the expression of above mentioned genes significantly increased in groups of metabolic syndrome treated with oil and extract compared to control and metabolic syndrome groups (p < 0.05).
CONCLUSION: It can be concluded that safflower seed extract and its oil can improve fructose-induced metabolic syndrome through antioxidant and anti-inflammatory effects, adjustment of homeostasis of trace elements, and enhancing the beta-oxidation capacity of the liver by increasing the expression of CD36, FAS, and CPT-1beta genes.


greenmedinfo--2020-12-17--Korean Superfood May Reduce Body Fat

Korean Superfood May Reduce Body Fat

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greenmedinfo--2020-12-17--Carthamus tinctorius L. Extract ameliorates cerebral ischemia-reperfusion injury.

We investigate the protective effect ofL .
( CTL , also known as Honghua in China or Safflower ) on cerebral ischemia-reperfusion and explored the possible mechanisms on regulating apoptosis and matrix metalloproteinases ( MMPs ) .
High-performance liquid chromatography method with diode array detection analysis was established to analyze the components of CTL .
Middle cerebral artery occlusion rats model was established to evaluate Neurological Function Score and hematoxylin-eosin staining , as well as triphenyltetrazolium was used to examine the infarction area ratio .
Transferase-mediated dUTP nick-end labeling was performed for the apoptosis .
Apoptosis-related factors , including B-cell @ @ @ @ @ @ @ Caspase3 , and MMPs-related MMP2 , MMP9 , tissue inhibitor of metalloproteinases 1 ( TIMP1 ) in ischemic brain , were assayed by Western blot , reverse transcription polymerase chain reaction , and immunohistochemistry .
The data showed that CTL ( 2 , 4 g crude drug/kg/d ) treatment could significantly reduce the ischemic damage in brain tissue and improve a significant neurological function score .
In addition , CTL could also attenuate apoptosis degree of brain tissues and regulate Bcl-2 , Bax , and Caspase 3 and also have a significant decrease @ @ @ @ @ @ @ significant increase of TIMP1 protein expression .
These findings indicated that regulation of CTL on apoptosis and MMPs contributed to its protective effect on ischemia/reperfusion injury .

We investigate the protective effect ofL. (CTL, also known as Honghua in China or Safflower) on cerebral ischemia-reperfusion and explored the possible mechanisms on regulating apoptosis and matrix metalloproteinases (MMPs). High-performance liquid chromatography method with diode array detection analysis was established to analyze the components of CTL. Middle cerebral artery occlusion rats model was established to evaluate Neurological Function Score and hematoxylin-eosin staining, as well as triphenyltetrazolium was used to examine the infarction area ratio. Transferase-mediated dUTP nick-end labeling was performed for the apoptosis. Apoptosis-related factors, including B-cell lymphoma-2 (Bcl-2), Bax and Caspase3, and MMPs-related MMP2, MMP9, tissue inhibitor of metalloproteinases 1 (TIMP1) in ischemic brain, were assayed by Western blot, reverse transcription polymerase chain reaction, and immunohistochemistry. The data showed that CTL (2, 4 g crude drug/kg/d) treatment could significantly reduce the ischemic damage in brain tissue and improve a significant neurological function score. In addition, CTL could also attenuate apoptosis degree of brain tissues and regulate Bcl-2, Bax, and Caspase 3 and also have a significant decrease on MMP-9 expression, followed by a significant increase of TIMP1 protein expression. These findings indicated that regulation of CTL on apoptosis and MMPs contributed to its protective effect on ischemia/reperfusion injury.


greenmedinfo--2020-12-17--Hydroxysafflor yellow A suppresses liver fibrosis induced by carbon tetrachloride with high-fat diet

Hydroxysafflor yellow A suppresses liver fibrosis induced by carbon tetrachloride with high-fat diet.

CONTEXT : One approach to protect against liver fibrosis is the use of herb-derived natural compounds , such as hydroxysafflor yellow A ( HSYA ) .
The antifibrosis effect of HYSA against liver fibrosis has been investigated ; however , its mechanisms have not yet been entirely revealed .
OBJECTIVES : To study the protective effects of HSYA on liver fibrosis induced by carbon tetrachloride ( CCl4 ) and a high-fat diet ( HFD ) , and to determine the mechanism of action of HSYA .
MATERIALS AND METHODS : CCl4 and HFD were used to mimic liver fibrosis in @ @ @ @ @ @ @ determined .
The antifibrosis effects of HSYA were evaluated and its mechanisms were investigated by histopathological analysis , immunohistochemical staining , enzyme-linked immunosorbent assays , real-time-PCR , and western blotting .
RESULTS : HSYA reduced CCl4- and HFD-mediated liver fibrosis and ameliorated serum biochemical indicator , downregulated the expression of tissue inhibitor of metalloproteinase-1 ( TIMP-1 ) ( 0.31 ± 0.03 protein , 0.59 ± 0.02 mRNA ) and transformin growth factor-β1 ( TGF-β1 ) ( 0.81 ± 0.02 protein , 0.58 ± 0.04 mRNA ) , and upregulated the expression of peroxisome @ @ @ @ @ @ @ ± 0.13 protein , 2.48 ± 0.19 mRNA ) and matrix metallopeptidases-2 ( MMP-2 ) ( 2.31 ± 0.16 protein , 2.79 ± 0.22 mRNA ) ( p DISCUSSION AND CONCLUSION : These data demonstrate a novel role for HSYA in inhibiting CCl4- and HFD-mediated liver fibrosis , and reveal that PPAR-γ and p38 MAPK signaling play pivotal roles in the prevention of liver fibrosis induced by CCl4 and HFD .

CONTEXT: One approach to protect against liver fibrosis is the use of herb-derived natural compounds, such as hydroxysafflor yellow A (HSYA). The antifibrosis effect of HYSA against liver fibrosis has been investigated; however, its mechanisms have not yet been entirely revealed.
OBJECTIVES: To study the protective effects of HSYA on liver fibrosis induced by carbon tetrachloride (CCl4) and a high-fat diet (HFD), and to determine the mechanism of action of HSYA.
MATERIALS AND METHODS: CCl4 and HFD were used to mimic liver fibrosis in rats, and serum biochemical indicators were determined. The antifibrosis effects of HSYA were evaluated and its mechanisms were investigated by histopathological analysis, immunohistochemical staining, enzyme-linked immunosorbent assays, real-time-PCR, and western blotting.
RESULTS: HSYA reduced CCl4- and HFD-mediated liver fibrosis and ameliorated serum biochemical indicator, downregulated the expression of tissue inhibitor of metalloproteinase-1 (TIMP-1) (0.31 ± 0.03 protein, 0.59 ± 0.02 mRNA) and transformin growth factor-β1 (TGF-β1) (0.81 ± 0.02 protein, 0.58 ± 0.04 mRNA), and upregulated the expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) (1.57 ± 0.13 protein, 2.48 ± 0.19 mRNA) and matrix metallopeptidases-2 (MMP-2) (2.31 ± 0.16 protein, 2.79 ± 0.22 mRNA) (p < 0.01, versus model group). These effects were significantly attenuated by PPAR-γ antagonist GW9662 via blocking the phosphorylation of p38 MAPK.
DISCUSSION AND CONCLUSION: These data demonstrate a novel role for HSYA in inhibiting CCl4- and HFD-mediated liver fibrosis, and reveal that PPAR-γ and p38 MAPK signaling play pivotal roles in the prevention of liver fibrosis induced by CCl4 and HFD.


greenmedinfo--2020-12-17--Hydroxysafflor yellow a attenuates small airway remodeling in a rat model of chronic obstructive pul

Hydroxysafflor yellow a attenuates small airway remodeling in a rat model of chronic obstructive pulmonary disease.

Our previous studies found that hydroxysafflor yellow A ( HSYA ) , an active ingredient in Carthamus tinctorius L. , @ @ @ @ @ .
In this study , we investigated the effect of HSYA on small airway remodeling @ @ @ @ @ chronic obstructive pulmonary disease ( COPD ) rat model induced by cigarette smoke and lipopolysaccharide @ @ @ @ @ is a common lesion in COPD characterized by thickening of the airway wall , mainly @ @ @ @ @ this study the thickness of the small airway was determined by total wall area/basement membrane @ @ @ @ @ Collagen deposition of the small airway was assessed by Masson 's trichrome staining .
HSYA @ @ @ @ @ collagen deposition of the small airway and inhibited transforming growth factorβ1 ( TGF-β1 ) mRNA @ @ @ @ @ rat .
In addition , HSYA inhibited the phosphorylation of p38 mitogen-activated protein kinases ( @ @ @ @ @ tissue of rat .
HSYA can attenuate experimentally induced airway remodeling and this attenuation may @ @ @ @ @ TGF-β1 expression .

Our previous studies found that hydroxysafflor yellow A (HSYA), an active ingredient in Carthamus tinctorius L., has anti-inflammatory and anti-fibrosis properties. In this study, we investigated the effect of HSYA on small airway remodeling (SAR) in a chronic obstructive pulmonary disease (COPD) rat model induced by cigarette smoke and lipopolysaccharide (LPS). SAR is a common lesion in COPD characterized by thickening of the airway wall, mainly by subepithelial fibrosis. In this study the thickness of the small airway was determined by total wall area/basement membrane perimeter (WAt/Pbm). Collagen deposition of the small airway was assessed by Masson's trichrome staining. HSYA significantly attenuated the thickening and collagen deposition of the small airway and inhibited transforming growth factorβ1 (TGF-β1) mRNA and protein expression in COPD rat. In addition, HSYA inhibited the phosphorylation of p38 mitogen-activated protein kinases (MAPK) in the lung tissue of rat. HSYA can attenuate experimentally induced airway remodeling and this attenuation may be attributed to suppression of TGF-β1 expression.


greenmedinfo--2020-12-17--Hydroxysafflor yellow A ameliorates lipopolysaccharide-induced acute lung injury.

Hydroxysafflor yellow A ( HSYA ) is a main bio-active compound important of a traditional Chinese medicine named Carthamus tinctorius L. and has been shown to possess various effects , especially anti-inflammatory benefits and potential protections against acute lung injury ( ALI ) in previous studies .
Therefore , in this present study , we aimed to evaluating effects of HSYA on lipopolysaccharide ( LPS ) -induced ALI in mice .
ALI was induced by intratracheal instillation of LPS into lung , and dexamethasone was used as a positive control .
Results demonstrated that HSYA abated LPS-induced pathological change and @ @ @ @ @ @ @ HSYA down-regulated both the ability of myeloperoxidase ( MPO ) in lung tissues and levels of inflammatory mediators including tumor necrosis factor ( TNF ) -α , interleukin ( IL ) -1β , IL-6 and IFN ( interferon ) -β in serum .
Moreover , HSYA prevented toll-like receptor 4 ( TLR4 ) , myeloid differentiation factor 88 ( MyD88 ) and TIR-domain-containing adapter-inducing interferon-β ( TRIF ) protein up-expressions .
In addition , the activations of mitogen-activated protein kinases including p38 , extracellular signal-regulated kinase ( ERK ) , c-Jun N-terminal kinase @ @ @ @ @ @ @ .
And also , the phosphorylations of interferon regulatory factor 3 ( IRF3 ) , translocation of nuclear factor kappa B ( NF-κB ) /p65 and inhibitory kappa B ( IκB ) -α were inhibitedby HSYA .
In conclusion , HSYA attenuated inflammatory response in ALI mice through inhibition of TLR 4-dependent signaling pathways .

Hydroxysafflor yellow A (HSYA) is a main bio-active compound important of a traditional Chinese medicine named Carthamus tinctorius L. and has been shown to possess various effects, especially anti-inflammatory benefits and potential protections against acute lung injury (ALI) in previous studies. Therefore, in this present study, we aimed to evaluating effects of HSYA on lipopolysaccharide (LPS)-induced ALI in mice. ALI was induced by intratracheal instillation of LPS into lung, and dexamethasone was used as a positive control. Results demonstrated that HSYA abated LPS-induced pathological change and attenuated lung vascular permeability and edema. HSYA down-regulated both the ability of myeloperoxidase (MPO) in lung tissues and levels of inflammatory mediators including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and IFN(interferon)-β in serum. Moreover, HSYA prevented toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and TIR-domain-containing adapter-inducing interferon-β (TRIF) protein up-expressions. In addition, the activations of mitogen-activated protein kinases including p38, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) were blocked by HSYA. And also, the phosphorylations of interferon regulatory factor 3 (IRF3), translocation of nuclear factor kappa B (NF-κB)/p65 and inhibitory kappa B (IκB)-α were inhibitedby HSYA. In conclusion, HSYA attenuated inflammatory response in ALI mice through inhibition of TLR 4-dependent signaling pathways.


greenmedinfo--2020-12-17--Neuroprotective effect of hydroxysafflor yellow A on 6-hydroxydopamine-induced Parkinson's disease.

Parkinson 's disease ( PD ) is a progressive neurodegenerative disorder affecting predominantly the dopaminergic mesotelencephalic system .
Enormous progress has been made in the treatment of PD .
Our previous study has shown that hydroxysafflor yellow A ( HSYA ) could attenuate the neurotoxicity induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice .
In the present work , we examined whether HSYA had the neuroprotective effect on dopaminergic neurons of substantia nigra in a rat model of PD .
Adult Sprague-Dawley rats were unilaterally injected with 6-hydroxydopamine ( 6-OHDA ) into the medial forebrain bundle .
The PD rats were treated with @ @ @ @ @ @ @ via caudal vein injection daily for 4 weeks .
Rotational tests showed that HSYA significantly attenuated apomorphine-induced turns in 6-OHDA-induced PD rats .
HSYA treatment resulted in a significant protection against the loss of tyrosine hydroxylase-positive cells .
Our data showed that HSYA also increased the levels of dopamine and its metabolites , glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor in striatum of PD rats .
In conclusion , these results supported a role for HSYA in preserving dopamine neuron integrity and motor function in a rodent model of PD , @ @ @ @ @ @ @ HSYA in this disease .

Parkinson's disease (PD) is a progressive neurodegenerative disorder affecting predominantly the dopaminergic mesotelencephalic system. Enormous progress has been made in the treatment of PD. Our previous study has shown that hydroxysafflor yellow A (HSYA) could attenuate the neurotoxicity induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice. In the present work, we examined whether HSYA had the neuroprotective effect on dopaminergic neurons of substantia nigra in a rat model of PD. Adult Sprague-Dawley rats were unilaterally injected with 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. The PD rats were treated with HSYA (2 or 8 mg/kg) via caudal vein injection daily for 4 weeks. Rotational tests showed that HSYA significantly attenuated apomorphine-induced turns in 6-OHDA-induced PD rats. HSYA treatment resulted in a significant protection against the loss of tyrosine hydroxylase-positive cells. Our data showed that HSYA also increased the levels of dopamine and its metabolites, glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor in striatum of PD rats. In conclusion, these results supported a role for HSYA in preserving dopamine neuron integrity and motor function in a rodent model of PD, and implied a potential neuroprotective role for HSYA in this disease.