greenmedinfo--2020-12-15--Therapeutic potential of hydroxysafflor yellow A on cardio-cerebrovascular diseases.

The incidence rate of cardio-cerebrovascular diseases ( CCVDs ) is increasing worldwide , causing an increasingly serious public health burden @ @ @ @ @ promising treatment options is thus becoming a pressing issue .
Hydroxysafflor yellow A ( HSYA @ @ @ @ @ main active quinochalcone-glycosides in the florets ofL.
, a medical and edible dual-purpose plant .
@ @ @ @ @ for its pharmacological actions in treating and/or managing CCVDs , such as myocardial and cerebral @ @ @ @ @ , vascular dementia , and traumatic brain injury , in massive preclinical studies .
In @ @ @ @ @ summarized the mode and mechanism of action of HSYA on CCVDs based on these preclinical @ @ @ @ @ of HSYA against CCVDs were presumed to reside mostly in its antioxidant , anti-inflammatory , @ @ @ @ @ on complex signaling pathways .

The incidence rate of cardio-cerebrovascular diseases (CCVDs) is increasing worldwide, causing an increasingly serious public health burden. The pursuit of new promising treatment options is thus becoming a pressing issue. Hydroxysafflor yellow A (HSYA) is one of the main active quinochalcone-glycosides in the florets ofL., a medical and edible dual-purpose plant. HSYA has attracted much interest for its pharmacological actions in treating and/or managing CCVDs, such as myocardial and cerebral ischemia, hypertension, atherosclerosis, vascular dementia, and traumatic brain injury, in massive preclinical studies. In this review, we briefly summarized the mode and mechanism of action of HSYA on CCVDs based on these preclinical studies. The therapeutic effects of HSYA against CCVDs were presumed to reside mostly in its antioxidant, anti-inflammatory, and neuroprotective roles by acting on complex signaling pathways.


greenmedinfo--2020-12-15--Hydroxysafflor yellow A attenuates hydrogen peroxide-induced oxidative damage.

Oxidative stress of endothelial cells is thought to be a principal cause that induces many cardiovascular diseases .
Hydroxysafflor yellow A ( HSYA ) is a major active component in traditional Chinese medicine safflower and has been used to cure ischemic cardiovascular diseases in China for many years .
This study aims to investigate whether HSYA has a repairing effect on oxidative damage of human umbilical vein endothelial cells ( HUVECs ) induced by HOand to provide a theoretical basis for the clinical treatment of cardiovascular diseases related to traditional Chinese medicine .
Based on the establishment of an HO-induced @ @ @ @ @ @ @ viability and proliferation rate were measured by the MTT assay and EdU staining .
The intracellular GSH/GSSG ratio and SOD activity were determined by kits .
The ROS level was detected by flow cytometry .
And the BAX , Bcl-2 , PTEN , and AKT expressions were evaluated with western blotting methods .
The results showed that HSYA treatment significantly attenuated the HO-induced HUVEC cell damage , increased the intracellular GSH/GSSG ratio and unit SOD activity also , and decreased the intracellular ROS levels .
Furthermore , HSYA increased the expressions of AKT @ @ @ @ @ @ @ of BAX and PTEN proteins .
These suggest that HSYA exerts repair effects on HO-induced oxidative damage in HUVECs , and the mechanisms may be related to the influence of BAX/Bcl-2 expression and AKT/PTEN signal pathway expression .

Oxidative stress of endothelial cells is thought to be a principal cause that induces many cardiovascular diseases. Hydroxysafflor yellow A (HSYA) is a major active component in traditional Chinese medicine safflower and has been used to cure ischemic cardiovascular diseases in China for many years. This study aims to investigate whether HSYA has a repairing effect on oxidative damage of human umbilical vein endothelial cells (HUVECs) induced by HOand to provide a theoretical basis for the clinical treatment of cardiovascular diseases related to traditional Chinese medicine. Based on the establishment of an HO-induced HUVEC oxidative injury model, the cell viability and proliferation rate were measured by the MTT assay and EdU staining. The intracellular GSH/GSSG ratio and SOD activity were determined by kits. The ROS level was detected by flow cytometry. And the BAX, Bcl-2, PTEN, and AKT expressions were evaluated with western blotting methods. The results showed that HSYA treatment significantly attenuated the HO-induced HUVEC cell damage, increased the intracellular GSH/GSSG ratio and unit SOD activity also, and decreased the intracellular ROS levels. Furthermore, HSYA increased the expressions of AKT and Bcl-2 proteins and inhibited the expressions of BAX and PTEN proteins. These suggest that HSYA exerts repair effects on HO-induced oxidative damage in HUVECs, and the mechanisms may be related to the influence of BAX/Bcl-2 expression and AKT/PTEN signal pathway expression.


greenmedinfo--2020-12-15--RFK, Jr. Warned FDA Three Months Ago About Ingredient in Pfizer COVID Vaccine

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greenmedinfo--2020-12-15--Antioxidant and antimicrobial potentials of seed oil from Carthamus tinctorius in the management of

Antioxidant and antimicrobial potentials of seed oil from Carthamus tinctorius in the management of skin injuries.

Infection of skin injuries by pathogenic microbial strains is generally associated if not treated with a lasting wound bed oxidative stress status , a delay in healing process , and even wound chronicity with several human health complications .
The aim of the current study was to explore the antioxidant and antimicrobial potentialities of safflower ( ) extracted oil from seeds by cold pressing which would be beneficial in the management of skin wounds .
Antioxidant capacity of the oil was evaluated ( scavenging ability against 1,1-diphenyl-2-picrylhydrazyl radical ( DPPH ) and 2,2'-azino-bis 3-ethylbenzothiazoline-6-sulfonic acid ( ABTS ) , and @ @ @ @ @ @ @ ) .
Total phenolic , total flavonoid , total carotenoid , and total chlorophyll contents were determined .
Antimicrobial activities of safflower oil were tested against 10 skin pathogenic microorganisms : 4 bacterial strains ( , , , and ) , 3 yeast species strains ( , , and ) , and 3 fungi species , , and ) .
A notable antioxidant capacity was demonstrated for the tested oil that exhibited moreover high antibacterial effects by both bacteriostatic and bactericidal pathways including lysozyme activity .
An antifungal effect was further observed on @ @ @ @ @ @ @ could be considered as a good natural alternative remedy in the management of skin wounds and their possible microbial infections .

Infection of skin injuries by pathogenic microbial strains is generally associated if not treated with a lasting wound bed oxidative stress status, a delay in healing process, and even wound chronicity with several human health complications. The aim of the current study was to explore the antioxidant and antimicrobial potentialities of safflower () extracted oil from seeds by cold pressing which would be beneficial in the management of skin wounds. Antioxidant capacity of the oil was evaluated (scavenging ability against 1,1-diphenyl-2-picrylhydrazyl radical (DPPH) and 2,2'-azino-bis 3-ethylbenzothiazoline-6-sulfonic acid (ABTS), and ferric reducing antioxidant power (FRAP)). Total phenolic, total flavonoid, total carotenoid, and total chlorophyll contents were determined. Antimicrobial activities of safflower oil were tested against 10 skin pathogenic microorganisms: 4 bacterial strains (,,, and), 3 yeast species strains (,, and), and 3 fungi species,, and). A notable antioxidant capacity was demonstrated for the tested oil that exhibited moreover high antibacterial effects by both bacteriostatic and bactericidal pathways including lysozyme activity. An antifungal effect was further observed on the spore's germination. Safflower oil could be considered as a good natural alternative remedy in the management of skin wounds and their possible microbial infections.


greenmedinfo--2020-12-15--The efficacy of processing strategies on the gastroprotective potentiality of Chenopodium quinoa see

The efficacy of processing strategies on the gastroprotective potentiality of Chenopodium quinoa seeds.

The current study has been conducted to evaluate the effect of different processing techniques on the 2,2-diphenyl-1-picrylhydrazyl ( DPPH ) scavenging capacity and the gastroprotective potential ofred seeds in acute gastric injury induced by absolute ethanol in rats .
Seven groups of female Sprague Dawley rats were assigned to normal and absolute ethanol ( absolute EtOH ) groups , given distilled water , reference control omeprazole ( OMP , 20 mg/kg ) , pressure-cooked quinoa seeds ( QP , 200 mg/kg ) , first stage-germinated quinoa seeds ( QG , 200 mg/kg ) , bacteria-fermented quinoa seeds ( QB , @ @ @ @ @ @ @ ( QF , 200 mg/kg ) .
One hour after treatment , all groups were given absolute ethanol , except for the normal control rats .
All animals were sacrificed after an additional hour , and the stomach tissues were examined for histopathology of hematoxylin and eosin staining , immunohistochemistry of cyclooxygenase 2 ( COX-2 ) , and nitric oxide synthase ( iNOS ) .
Stomach homogenates were evaluated for oxidative stress parameters and prostaglandin E ( PGE ) .
Gene expression was performed for gastric tumor necrosis factor alpha ( TNF- ) @ @ @ @ @ @ @ ( NF-kB ) .
QB and QG recorded the highest DPPH scavengers compared to QF and QP .
The gastroprotective potential of QB was comparable to that of OMP , followed by QF , then QG , and QP as confirmed by the histopathology , immunohistochemistry , and gene expression assessments .
In conclusion , differently processed red quinoa seeds revealed variable antioxidant capacity and gastroprotective potential , while the bacterial fermented seeds ( QB ) showed the highest potential compared to the other processing techniques .
These results might offer promising new @ @ @ @ @ @ @ injury .

The current study has been conducted to evaluate the effect of different processing techniques on the 2,2-diphenyl-1-picrylhydrazyl (DPPH) scavenging capacity and the gastroprotective potential ofred seeds in acute gastric injury induced by absolute ethanol in rats. Seven groups of female Sprague Dawley rats were assigned to normal and absolute ethanol (absolute EtOH) groups, given distilled water, reference control omeprazole (OMP, 20 mg/kg), pressure-cooked quinoa seeds (QP, 200 mg/kg), first stage-germinated quinoa seeds (QG, 200 mg/kg),bacteria-fermented quinoa seeds (QB, 200 mg/kg), andfungus-fermented quinoa seeds (QF, 200 mg/kg). One hour after treatment, all groups were given absolute ethanol, except for the normal control rats. All animals were sacrificed after an additional hour, and the stomach tissues were examined for histopathology of hematoxylin and eosin staining, immunohistochemistry of cyclooxygenase 2(COX-2), and nitric oxide synthase (iNOS). Stomach homogenates were evaluated for oxidative stress parameters and prostaglandin E(PGE). Gene expression was performed for gastric tumor necrosis factor alpha (TNF-) and nuclear factor kappa of B cells (NF-kB). QB and QG recorded the highest DPPH scavengers compared to QF and QP. The gastroprotective potential of QB was comparable to that of OMP, followed by QF, then QG, and QP as confirmed by the histopathology, immunohistochemistry, and gene expression assessments. In conclusion, differently processed red quinoa seeds revealed variable antioxidant capacity and gastroprotective potential, while the bacterial fermented seeds (QB) showed the highest potential compared to the other processing techniques. These results might offer promising new therapy in the treatment of acute gastric injury.


greenmedinfo--2020-12-15--Dietary quinoa polysaccharides ameliorate high-fat diet-induced hyperlipidemia and modulate gut micr

Dietary quinoa polysaccharides ameliorate high-fat diet-induced hyperlipidemia and modulate gut microbiota.

As the high nutritional and functional values of quinoa acknowledged , the increasing researches focus on the bioactivities and related mechanisms of its abundant carbohydrates .
Herein , the beneficial effects of the soluble polysaccharide fraction from quinoa was investigated to lower the serum lipid of rats treated by high-fat diet ( HFD ) and call the disordered gut microbiota back .
The polysaccharide faction was firstly extracted by ultrasonic-assisted extraction technology ( yield of 9.65 % ) and characterized of the monosaccharide composition with glucose and arabinose ( 1.17:1 , molar ratio ) .
And then , the oral @ @ @ @ @ @ @ 600 mg·kg·dayfor 8 weeks remarkably alleviated dyslipidemia by decreasing the levels of serum total triglyceride ( TG ) , low density lipoprotein cholesterol ( LDL-C ) , malondialdehyde ( MDA ) , total glutamic pyruvic transaminase ( ALT ) and glutamic oxaloacetic transaminase ( AST ) in rats fed with HFD , as well as the reducedhepatic lipid accumulation .
Meanwhile , the relative abundance of gut microbiota could be disordered by the long term of HFD .
Nevertheless , dietary supplementation of quinoa polysaccharide could enhance species richness and regulate the gut @ @ @ @ @ @ @ of Firmicutes and Bacteroides , the relative abundance of Proteobacteria .
Meanwhile , Sequencing of 16S rRNA gene revealed that intake of quinoa polysaccharide decreased the relative abundances of Desulfovibrio and Allobaculum , which were positively correlated with serum lipid profiles and beneficial to lessen intestinal inflammation .
Taken together , the present study demonstrated that quinoa polysaccharide supplementation could ameliorate the hyperlipidemia induced by HFD in association with modulating gut microbiota in a positive way .

As the high nutritional and functional values of quinoa acknowledged, the increasing researches focus on the bioactivities and related mechanisms of its abundant carbohydrates. Herein, the beneficial effects of the soluble polysaccharide fraction from quinoa was investigated to lower the serum lipid of rats treated by high-fat diet (HFD) and call the disordered gut microbiota back. The polysaccharide faction was firstly extracted by ultrasonic-assisted extraction technology (yield of 9.65%) and characterized of the monosaccharide composition with glucose and arabinose (1.17:1, molar ratio). And then, the oral administration of quinoa polysaccharide of 300 mg·kg·dayand 600 mg·kg·dayfor 8 weeks remarkably alleviated dyslipidemia by decreasing the levels of serum total triglyceride (TG), low density lipoprotein cholesterol (LDL-C), malondialdehyde (MDA), total glutamic pyruvic transaminase (ALT) and glutamic oxaloacetic transaminase (AST) in rats fed with HFD, as well as the reducedhepatic lipid accumulation. Meanwhile, the relative abundance of gut microbiota could be disordered by the long term of HFD. Nevertheless, dietary supplementation of quinoa polysaccharide could enhance species richness and regulate the gut microbiota community structure, reducing the ratio of Firmicutes and Bacteroides, the relative abundance of Proteobacteria. Meanwhile, Sequencing of 16S rRNA gene revealed that intake of quinoa polysaccharide decreased the relative abundances of Desulfovibrio and Allobaculum, which were positively correlated with serum lipid profiles and beneficial to lessen intestinal inflammation. Taken together, the present study demonstrated that quinoa polysaccharide supplementation could ameliorate the hyperlipidemia induced by HFD in association with modulating gut microbiota in a positive way.


greenmedinfo--2020-12-15--Phenolic profile, antioxidant activity, and ameliorating efficacy of Chenopodium quinoa sprouts agai

Phenolic profile, antioxidant activity, and ameliorating efficacy of Chenopodium quinoa sprouts against CCl 4-induced oxidative stress.

Quinoa ( ) is classified as one of the pseudo-cereal grains rich in both macronutrients and micronutrients .
This study tracks changes in the polyphenol composition of red quinoa ( RQ ) and yellow quinoa ( YQ ) seeds during germination .
The antioxidant bioactivity of raw and germinated seed was also determined in vitro .
Phenolic acids and their derivatives and flavonoids were identified by using HPLC-DAD and quantified after 0 , 3 , and 6 days of germination .
Subsequently , the extracts of 6-day-old quinoa sprouts were prepared to biologically evaluate their functional properties against CCl-induced oxidative @ @ @ @ @ @ @ that antioxidant activity ( AOA ) of total phenolic compounds ( TPC ) , and flavonoids significantly increased in RQ and YQ sprouts during germination up to 9 days .
RQ sprouts exhibited stronger bioactive compound diversity than YQ sprouts as observed in HPLC analysis .
Among the 11 and 8 quantified polyphenols , ferulic acid and quercetin were predominant phenolic acid and flavonoid in RQ and YQ sprouts , respectively .
After 6 days of germination , 16 and 8 polyphenols were detected and quantified in RQ and YQ sprouts , respectively @ @ @ @ @ @ @ at a dose of 30 mg of Gallic acid Equivalent ( GAE ) kgsignificantly reduced fasting blood glucose ( FBG ) , alanine aminotransferase ( ALT ) , aspartate aminotransferase AST , and total bilirubin ( TIBIL ) and improved liver inflammation .
Furthermore , RQ and YQ sprouts improved the blood profile by significantly decreasing low-density lipoproteins ( LDL ) and very low-density lipoproteins ( VLDL ) and increasing high-density lipoproteins ( HDL ) .
Moreover , RQ and YQ sprout extracts significantly reduced malonaldehyde ( MDA ) and efficiently enhanced the @ @ @ @ @ @ @ dismutase ( SOD ) activities in oxidative stress-induced rats as compared to CCl-rats .
In conclusion , red quinoa sprouts ( RQS ) and yellow quinoa sprouts ( YQS ) provide naturally synthesized polyphenols , possessing superior antioxidant activity , and their ethanolic extracts have promising effects and potential health benefits to counter induced oxidative stress .
Incorporating quinoa sprouts as functional food ingredients should be considered and scaling-up its production is beneficial .

Quinoa () is classified as one of the pseudo-cereal grains rich in both macronutrients and micronutrients. This study tracks changes in the polyphenol composition of red quinoa (RQ) and yellow quinoa (YQ) seeds during germination. The antioxidant bioactivity of raw and germinated seed was also determined in vitro. Phenolic acids and their derivatives and flavonoids were identified by using HPLC-DAD and quantified after 0, 3, and 6 days of germination. Subsequently, the extracts of 6-day-old quinoa sprouts were prepared to biologically evaluate their functional properties against CCl-induced oxidative stress in rats. The results indicated that antioxidant activity (AOA) of total phenolic compounds (TPC), and flavonoids significantly increased in RQ and YQ sprouts during germination up to 9 days. RQ sprouts exhibited stronger bioactive compound diversity than YQ sprouts as observed in HPLC analysis. Among the 11 and 8 quantified polyphenols, ferulic acid and quercetin were predominant phenolic acid and flavonoid in RQ and YQ sprouts, respectively. After 6 days of germination, 16 and 8 polyphenols were detected and quantified in RQ and YQ sprouts, respectively. Interestingly, the treatment of rats at a dose of 30 mg of Gallic acid Equivalent (GAE) kgsignificantly reduced fasting blood glucose (FBG), alanine aminotransferase (ALT), aspartate aminotransferase AST, and total bilirubin (TIBIL) and improved liver inflammation. Furthermore, RQ and YQ sprouts improved the blood profile by significantly decreasing low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL) and increasing high-density lipoproteins (HDL). Moreover, RQ and YQ sprout extracts significantly reduced malonaldehyde (MDA) and efficiently enhanced the reduced glutathione (GSH) and superoxide dismutase (SOD) activities in oxidative stress-induced rats as compared to CCl-rats. In conclusion, red quinoa sprouts (RQS) and yellow quinoa sprouts (YQS) provide naturally synthesized polyphenols, possessing superior antioxidant activity, and their ethanolic extracts have promising effects and potential health benefits to counter induced oxidative stress. Incorporating quinoa sprouts as functional food ingredients should be considered and scaling-up its production is beneficial.


greenmedinfo--2020-12-15--Dietary Salvia hispanica L. reduces cardiac oxidative stress of dyslipidemic insulin-resistant rats.

L. , commonly known as chia seed , has beneficial effects upon some signs of metabolic syndrome ( MS ) , such as dyslipidemia and insulin resistance .
However , its action on cardiac oxidative stress associated with MS remains unknown .
The goal of this study was to analyze the possible beneficial effects of chia seed ( variety Salba ) upon the oxidative stress of left ventricle heart muscle ( LV ) of a well-established dyslipidemic insulin-resistant rat model induced by feeding them a sucrose-rich diet ( SRD ) .
Male Wistar rats received an SRD for 3 months @ @ @ @ @ @ @ months , half of the animals continued with the SRD , while the other half received the SRD containing chia as the source of dietary fat instead corn oil ( SRD+chia ) .
In the LV of SRD-fed rats , chia seed improved/reverted the depleted activity of antioxidant enzymes glutathione peroxidase , superoxide dismutase ( SOD ) , and catalase , and amelioratedmessenger RNA ( mRNA ) levels increasing the expression of the nuclear factor erythroid 2-related factor 2 ( Nrf2 ) .
Improved the glutathione redox estate , reactive oxygen species , @ @ @ @ @ @ @ thesubunit mRNA level .
Furthermore , chia normalized hypertension and plasma levels of pro-inflammatory cytokines and oxidative stress biomarkers .
The findings show that chia seed intake impacts positively upon oxidative imbalance of LV of dyslipidemic insulin-resistant rats.Healthy effects of chia seed involve an improvement of cardiac antioxidant defenses through Nrf2 induction .
Chia seed intake reduces cardiac oxidative stress markers of dyslipidemic insulin-resistant rats .
Dietary chia seed restores cardiac unbalanced redox state of dyslipidemic insulin-resistant rats .

L., commonly known as chia seed, has beneficial effects upon some signs of metabolic syndrome (MS), such as dyslipidemia and insulin resistance. However, its action on cardiac oxidative stress associated with MS remains unknown. The goal of this study was to analyze the possible beneficial effects of chia seed (variety Salba) upon the oxidative stress of left ventricle heart muscle (LV) of a well-established dyslipidemic insulin-resistant rat model induced by feeding them a sucrose-rich diet (SRD). Male Wistar rats received an SRD for 3 months. After that, for 3 additional months, half of the animals continued with the SRD, while the other half received the SRD containing chia as the source of dietary fat instead corn oil (SRD+chia). In the LV of SRD-fed rats, chia seed improved/reverted the depleted activity of antioxidant enzymes glutathione peroxidase, superoxide dismutase (SOD), and catalase, and amelioratedmessenger RNA (mRNA) levels increasing the expression of the nuclear factor erythroid 2-related factor 2 (Nrf2). Improved the glutathione redox estate, reactive oxygen species, and thiobarbituric acid reactive substances contents normalizing thesubunit mRNA level. Furthermore, chia normalized hypertension and plasma levels of pro-inflammatory cytokines and oxidative stress biomarkers. The findings show that chia seed intake impacts positively upon oxidative imbalance of LV of dyslipidemic insulin-resistant rats.Healthy effects of chia seed involve an improvement of cardiac antioxidant defenses through Nrf2 induction. Chia seed intake reduces cardiac oxidative stress markers of dyslipidemic insulin-resistant rats. Dietary chia seed restores cardiac unbalanced redox state of dyslipidemic insulin-resistant rats.


greenmedinfo--2020-12-15--Chia oil induces browning of white adipose tissue in high-fat diet-induced obese mice.

Previous research suggests that omega-3 fatty acids from animal origin may promote the browning of subcutaneous white adipose tissue .
@ @ @ @ @ a plant oil ( chia , Salvia hispanica L. ) rich in alpha-linolenic fatty acid @ @ @ @ @ would promote browning and improve glucose metabolism in animals subjected to an obesogenic diet .
@ @ @ @ @ = 28 ) were divided into 4 groups : C : control diet ; H @ @ @ @ @ : animals in the H group supplemented with chia oil after reaching obesity ; HCW @ @ @ @ @ on a high-fat diet supplemented with chia oil .
Glucose tolerance , inflammatory markers , @ @ @ @ @ proteins involved in the browning process were examined .
When supplemented since weaning , chia @ @ @ @ @ promoted the browning process and a healthier phenotype .
Results of this study suggested that @ @ @ @ @ protect against the development of obesity-related diseases .

Previous research suggests that omega-3 fatty acids from animal origin may promote the browning of subcutaneous white adipose tissue. We evaluated if supplementation with a plant oil (chia, Salvia hispanica L.) rich in alpha-linolenic fatty acid (C18:3;ω-3) would promote browning and improve glucose metabolism in animals subjected to an obesogenic diet. Swiss male mice (n = 28) were divided into 4 groups: C: control diet; H: high-fat diet; HC: animals in the H group supplemented with chia oil after reaching obesity; HCW: animals fed since weaning on a high-fat diet supplemented with chia oil. Glucose tolerance, inflammatory markers, and expression of genes and proteins involved in the browning process were examined. When supplemented since weaning, chia oil improved glucose metabolism and promoted the browning process and a healthier phenotype. Results of this study suggested that chia oil has potential to protect against the development of obesity-related diseases.


greenmedinfo--2020-12-15--C. quinoa and S. hispanica seeds provide immunonutritional agonists to selectively polarize macropha

C. quinoa and S. hispanica seeds provide immunonutritional agonists to selectively polarize macrophages.

Diet-related immunometabolic-based diseases are associated with chronic inflammation in metabolic tissues , and infiltrated macrophages have been suggested as mediators for tissue- damaging inflammation .
Growing evidence implicatesandL .
as important contributors to immunonutritional health .
However , the functional roles of the immunonutritional protease inhibitors ( PPIs ) found in these crops on the macrophages ' metabolic and phenotypic adaptation remain to be elucidated .
The salt soluble fraction of proteins was extracted and analyzed confirming the presence of 11S and 2S albumin .
The < 30 kDa fraction of the extract from both crops was subjected to simulated @ @ @ @ @ @ @ ) polypeptides from 2S-type of proteins were found , along with the 2S albumin ( 13 kDa ) forin the bioaccessible fraction ( BAF ) .
Using human-like macrophage cells to deepen our understanding of the modulatory effects of this BAF , FACS analyses revealed their potential as TLR4 agonists , favoring increased phenotypic CD68/CD206 ratios .
The results of mitochondrial stress tests showed that cells increased oxygen consumption rates and non-mitochondrial respiration , confirming negligible deleterious effects on mitochondrial function .
At molecular-level , adaptation responses shed light on changes showing biological @ @ @ @ @ @ @ immunometabolic effects triggered by PPIs can be a part of a tailored nutritional intervention strategy in immunometabolic-based diseases .

Diet-related immunometabolic-based diseases are associated with chronic inflammation in metabolic tissues, and infiltrated macrophages have been suggested as mediators for tissue- damaging inflammation. Growing evidence implicatesandL. as important contributors to immunonutritional health. However, the functional roles of the immunonutritional protease inhibitors (PPIs) found in these crops on the macrophages' metabolic and phenotypic adaptation remain to be elucidated. The salt soluble fraction of proteins was extracted and analyzed confirming the presence of 11S and 2S albumin. The<30 kDa fraction of the extract from both crops was subjected to simulated gastrointestinal digestion, where (RP-LC-MS/MS analyses) polypeptides from 2S-type of proteins were found, along with the 2S albumin (13 kDa) forin the bioaccessible fraction (BAF). Using human-like macrophage cells to deepen our understanding of the modulatory effects of this BAF, FACS analyses revealed their potential as TLR4 agonists, favoring increased phenotypic CD68/CD206 ratios. The results of mitochondrial stress tests showed that cells increased oxygen consumption rates and non-mitochondrial respiration, confirming negligible deleterious effects on mitochondrial function. At molecular-level, adaptation responses shed light on changes showing biological correlation with TLR4 signaling. The resulting immunometabolic effects triggered by PPIs can be a part of a tailored nutritional intervention strategy in immunometabolic-based diseases.


greenmedinfo--2020-12-15--Neuroprotective effect from Salvia hispanica peptide fractions on pro-inflammatory modulation of HMC

Neuroprotective effect from Salvia hispanica peptide fractions on pro-inflammatory modulation of HMC3 microglial cells.

Neuroinflammation plays a critical role in the neurodegenerative disease 's development , where microglia 's act an important role in the mechanisms of response to neuronal damage .
In the present research , the neuroprotective effect from Salvia hispanica peptide fractions on the proinflammatory modulation on HMC3 microglial cells was evaluated .
From the enzymatic hydrolysis of a protein-rich fraction from S. hispanica seeds , three peptide fractions ( < 1 , 1-3 and 3-5 kDa ) were obtained , from which its neuroprotective and anti-inflammatory effect was determined on the production of proinflammatory mediators on HMC3 cells .
The @ @ @ @ @ @ @ ( 79.04 % ) , associated with the decrease in ROS cell production ( 51.3 ± 2.3 % ) .
Likewise , F1-3 kDa at 50 µg/ml , presented the highest reduction percentages of NO ( 33.1 ± 2.30 % ) , TNFα ( 26.4 ± 1.1 % ) and IL6 ( 17.36 ± 1.6 % ) .
F1-3 kDa exhibited a neuroprotective effect in HMC3 cells associated with its antioxidant and anti-inflammatory effect .
PRACTICAL APPLICATIONS : Currently , neurodegenerative diseases represent a global health problem , so the search for bioactive @ @ @ @ @ @ @ the prevention and treatment of this group of diseases .
Peptide research with an effect on the proinflammatory and prooxidant mediator 's reduction presentsa potential application in the functional food 's development aimed at the treatment of chronic diseases , that have oxidative stress and inflammation as their etiological factor .
The present research adds to the scientific evidence of the potential benefits of bioactive peptides obtained from chia seeds .
The results correlate with the main health benefits of whole chia seed in humans , such as antioxidant , anti-inflammatory , hypoglycemic @ @ @ @ @ @ @ associated with the protein and peptide composition of chia , which increases its added value as food .

Neuroinflammation plays a critical role in the neurodegenerative disease's development, where microglia's act an important role in the mechanisms of response to neuronal damage. In the present research, the neuroprotective effect from Salvia hispanica peptide fractions on the proinflammatory modulation on HMC3 microglial cells was evaluated. From the enzymatic hydrolysis of a protein-rich fraction from S. hispanica seeds, three peptide fractions (<1, 1-3 and 3-5 kDa) were obtained, from which its neuroprotective and anti-inflammatory effect was determined on the production of proinflammatory mediators on HMC3 cells. The F1-3 kDa exhibited the greatest protective effect (79.04%), associated with the decrease in ROS cell production (51.3 ± 2.3%). Likewise, F1-3 kDa at 50 µg/ml, presented the highest reduction percentages of NO (33.1 ± 2.30%), TNFα (26.4 ± 1.1%) and IL6 (17.36 ± 1.6%). F1-3 kDa exhibited a neuroprotective effect in HMC3 cells associated with its antioxidant and anti-inflammatory effect. PRACTICAL APPLICATIONS: Currently, neurodegenerative diseases represent a global health problem, so the search for bioactive compounds with neuroprotective effect is useful in the prevention and treatment of this group of diseases. Peptide research with an effect on the proinflammatory and prooxidant mediator's reduction presentsa potential application in the functional food's development aimed at the treatment of chronic diseases, that have oxidative stress and inflammation as their etiological factor. The present research adds to the scientific evidence of the potential benefits of bioactive peptides obtained from chia seeds. The results correlate with the main health benefits of whole chia seed in humans, such as antioxidant, anti-inflammatory, hypoglycemic and hypotensive capacity. This relationship is associated with the protein and peptide composition of chia, which increases its added value as food.


greenmedinfo--2020-12-15--Macrophage recruitment to adipocyte and the development of obesity associated inflammation was suppr

Macrophage recruitment to adipocyte and the development of obesity associated inflammation was suppressed by chia seeds.

The present study aimed to determine the role ofL.
, ( chia seed ) fatty acid content in adipocyte lipid accumulation and human macrophage immunoregulatory potential .
Chia seed fatty acid was extracted using hexane by the cold percolation method .
A gas chromatography-mass spectrometry ( GC-MS ) analysis showed a 3:1 ratio of omega 3 and omega 6 fatty acid composition and it was more beneficial for human health .
We treated it with increasing concentrations ( 0-6.4μg/mL ) of chia seed fatty acid extract to determine the cytotoxicity on the preadipocytes and macrophage ; no significant cytotoxicity was @ @ @ @ @ @ @ and 0.4 μg/mL doses , significantly arrested adipocyte hypertrophy and macrophage foam cell development .
The gene expression levels of adipocyte confirmed the increased expression of adipocyte mitochondrial thermogenesis related genes , such as uncoupling protein-1 ( UCP-1 ) , peroxisome proliferator activated receptor gamma coactivator 1 alpha ( PPARγC1α ) and PR domain containing 16 ( PRDM16 ) ; and the down regulated expression of the lipid synthesis related gene sterol regulatory element binding of protein-1c ( SREBP-1c ) .
In addition , adipogenesis related genes , such as the proliferator activated @ @ @ @ @ @ @ binding protein ( C/EBPα ) expressions , have been down regulated by chia seed treatment .
Macrophage treated with chia seed-treated adipocyte condition media significantly inhibited the obesity associated inflammatory genes and protein expression levels , such as monocyte chemo attractant protein-1 ( MCP-1 ) , prostaglandins E2 , interleukin-6 , plasminogen activator inhibitor-1 ( PAI-1 ) and tumor necrosis factor-α ( TNF-α ) .
In conclusion , a 3:1 ratio of omega 3 and omega 6 fatty acid composition of chia seed fatty acid content potentially inhibits lipid accumulation , and enhanced @ @ @ @ @ @ @ PRDM16 expression .
Macrophage recruitment to adipocyte and the development ofobesity associated inflammation was suppressed by chia seeds .

The present study aimed to determine the role ofL., (chia seed) fatty acid content in adipocyte lipid accumulation and human macrophage immunoregulatory potential. Chia seed fatty acid was extracted using hexane by the cold percolation method. A gas chromatography-mass spectrometry (GC-MS) analysis showed a 3:1 ratio of omega 3 and omega 6 fatty acid composition and it was more beneficial for human health. We treated it with increasing concentrations (0-6.4μg/mL) of chia seed fatty acid extract to determine the cytotoxicity on the preadipocytes and macrophage; no significant cytotoxicity was observed. Chia seed, in 0.2 and 0.4 μg/mL doses, significantly arrested adipocyte hypertrophy and macrophage foam cell development. The gene expression levels of adipocyte confirmed the increased expression of adipocyte mitochondrial thermogenesis related genes, such as uncoupling protein-1 (UCP-1), peroxisome proliferator activated receptor gamma coactivator 1 alpha (PPARγC1α) and PR domain containing 16 (PRDM16); and the down regulated expression of the lipid synthesis related gene sterol regulatory element binding of protein-1c (SREBP-1c). In addition, adipogenesis related genes, such as the proliferator activated receptor γ (PPARγ) and CCAAT/enhancer binding protein (C/EBPα) expressions, have been down regulated by chia seed treatment. Macrophage treated with chia seed-treated adipocyte condition media significantly inhibited the obesity associated inflammatory genes and protein expression levels, such as monocyte chemo attractant protein-1 (MCP-1), prostaglandins E2, interleukin-6, plasminogen activator inhibitor-1 (PAI-1) and tumor necrosis factor-α (TNF-α). In conclusion, a 3:1 ratio of omega 3 and omega 6 fatty acid composition of chia seed fatty acid content potentially inhibits lipid accumulation, and enhanced fatty acid oxidation, via UCP-1 and PRDM16 expression. Macrophage recruitment to adipocyte and the development ofobesity associated inflammation was suppressed by chia seeds.


greenmedinfo--2020-12-15--Chia-supplemented diet ameliorates non-alcoholic fatty liver disease and its metabolic abnormalities

Chia-supplemented diet ameliorates non-alcoholic fatty liver disease and its metabolic abnormalities in humans.

BACKGROUND : Non-alcoholic fatty liver disease ( NAFLD ) is a public health problem lacking an approved pharmacological treatment .
Omega-3 fatty acids have shown to reverse NAFLD .
Chia is a seed rich inα-linolenic acid ( ALA ) , antioxidants , and fiber ; therefore , it could be useful to treat NAFLD .
METHODS : In a single arm experimental design study , the effect of 25 g/day of milled chia was assessed in 25 patients with NAFLD .
After two weeks of dietary stabilization ( basal condition ) and eight weeks of a chia-supplemented isocaloric diet , @ @ @ @ @ @ @ abdominal fat ( VAF ) were measured by computed tomography .
Lipids , lipoproteins , free fatty acids ( FFA ) , and ALA plasma concentrations were also determined .
RESULTS : Dietary chia supplementation induced an increase in plasma ALA concentration ( 75 % ) and dietary fiber ( 55 % ) consumption .
After chia supplementation , VAF ( 9 % ) , body weight ( 1.4 % ) , total cholesterol ( 2.5 % ) , non-high density lipoprotein cholesterol ( 3.2 % ) , and circulating FFA ( 8 @ @ @ @ @ @ @ regressed in 52 % of the treated patients ( P CONCLUSIONS : The results of the present study show that 25 g/day of milled chia ameliorates NAFLD .
Chia is an accessible vegetal source of omega-3 fatty acids , antioxidants , and fiber , which could have the potential to prevent metabolic abnormalities in NAFLD patients .
Considering that there is no pharmacological treatment approved for NAFLD , the findings of the present study suggest that a chia-supplemented diet could be an innovative alternative to control this disease .
RETROSPECTIVELY REGISTERED : https @ @ @

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a public health problem lacking an approved pharmacological treatment. Omega-3 fatty acids have shown to reverse NAFLD. Chia is a seed rich inα-linolenic acid (ALA), antioxidants, and fiber; therefore, it could be useful to treat NAFLD.
METHODS: In a single arm experimental design study, the effect of 25 g/day of milled chia was assessed in 25 patients with NAFLD. After two weeks of dietary stabilization (basal condition) and eight weeks of a chia-supplemented isocaloric diet, liver:spleen attenuation index and visceral abdominal fat (VAF) were measured by computed tomography. Lipids, lipoproteins, free fatty acids (FFA), and ALA plasma concentrations were also determined.
RESULTS: Dietary chia supplementation induced an increase in plasma ALA concentration (75%) and dietary fiber (55%) consumption. After chia supplementation, VAF (9%), body weight (1.4%), total cholesterol (2.5%), non-high density lipoprotein cholesterol (3.2%), and circulating FFA (8%) decreased. Furthermore, NAFLD regressed in 52% of the treated patients (P < 0.05 for all).
CONCLUSIONS: The results of the present study show that 25 g/day of milled chia ameliorates NAFLD. Chia is an accessible vegetal source of omega-3 fatty acids, antioxidants, and fiber, which could have the potential to prevent metabolic abnormalities in NAFLD patients. Considering that there is no pharmacological treatment approved for NAFLD, the findings of the present study suggest that a chia-supplemented diet could be an innovative alternative to control this disease. RETROSPECTIVELY REGISTERED: https://clinicaltrials.gov/show/NCT03942822.


greenmedinfo--2020-12-15--Chenopodium Quinoa and Salvia Hispanica provide immunonutritional agonists to ameliorate hepatocarci

Chenopodium Quinoa and Salvia Hispanica provide immunonutritional agonists to ameliorate hepatocarcinoma severity under a high-fat diet.

Complex interactions between immunonutritional agonist and high fat intake ( HFD ) , the immune system and finally gut microbiota are important determinants of hepatocarcinoma ( HCC ) severity .
The ability of immunonutritional agonists to modulate major aspects such as liver innate immunity and inflammation and alterations in major lipids profile as well as gut microbiota during HCC development is poorly understood.H NMR has been employed to assess imbalances in saturated fatty acids , MUFA and PUFA , which were associated to variations in iron homeostasis .
These effects were dependent on the botanical nature ( vs.L . )
@ @ @ @ @ @ @ that immunonutritional agonists ' promoted resistance to hepatocarcinogenesis under pro-tumorigenic inflammation reflected , at a different extent , in increased proportions of F4/80cells in injured livers as well as positive trends of accumulated immune mediators ( CD68/CD206 ratio ) in intestinal tissue .
Administration of all immunonutritional agonists caused similar variations of fecal microbiota , towards a lower obesity-inducing potential than animals only fed a HFD .
Modulation oftocontents restored the induction of microbial metabolites to improve epithelial barrier function , showing an association with liver saturated fatty acids and the MUFA and @ @ @ @ @ @ @ provide novel findings supporting beneficial immunometabolic effects targeting hepatocarcinogenesis , influencing innate immunity within the gut-liver axis , and providing novel insights into their immunomodulatory activity .

Complex interactions between immunonutritional agonist and high fat intake (HFD), the immune system and finally gut microbiota are important determinants of hepatocarcinoma (HCC) severity. The ability of immunonutritional agonists to modulate major aspects such as liver innate immunity and inflammation and alterations in major lipids profile as well as gut microbiota during HCC development is poorly understood.H NMR has been employed to assess imbalances in saturated fatty acids, MUFA and PUFA, which were associated to variations in iron homeostasis. These effects were dependent on the botanical nature (vs.L.) of the compounds. The results showed that immunonutritional agonists' promoted resistance to hepatocarcinogenesis under pro-tumorigenic inflammation reflected, at a different extent, in increased proportions of F4/80cells in injured livers as well as positive trends of accumulated immune mediators (CD68/CD206 ratio) in intestinal tissue. Administration of all immunonutritional agonists caused similar variations of fecal microbiota, towards a lower obesity-inducing potential than animals only fed a HFD. Modulation oftocontents restored the induction of microbial metabolites to improve epithelial barrier function, showing an association with liver saturated fatty acids and the MUFA and PUFA fractions. Collectively, these data provide novel findings supporting beneficial immunometabolic effects targeting hepatocarcinogenesis, influencing innate immunity within the gut-liver axis, and providing novel insights into their immunomodulatory activity.


greenmedinfo--2020-12-16--Effects of hydroxysafflor yellow A on the PI3K/AKT pathway and apoptosis of pancreatic β-Cells in ty

Effects of hydroxysafflor yellow A on the PI3K/AKT pathway and apoptosis of pancreatic β-Cells in type 2 diabetes mellitus.

Background and Aim : Type 2 diabetes mellitus ( T2DM ) , a complex metabolic disease , has become a major public health issue around the world .
Hydroxysafflor yellow A ( HSYA ) is the major active chemical ingredient of .
( safflower ) , which is widely used in patients with cardiovascular and cerebrovascular diseases in China .
The aim of this study was to investigate the anti-diabetic effect and potential mechanism of HSYA on the high-fat diet ( HFD ) and streptozotocin ( STZ- ) -induced T2DM rats .
Materials and Methods : T2DM rats were induced @ @ @ @ @ @ @ ) for four weeks followed by intraperitoneal injection of a low dose of streptozocin ( 35mg/kg ) .
The T2DM rats were treated with HSYA ( 120mg/kg ) or metformin ( 90mg/kg ) for eight weeks .
Biochemical analysis , histological analysis and Western blot analysis were conducted after 8 weeks of intervention .
Results : The treatment with HSYA evidently reduced fasting-blood glucose and insulin resistance in T2DM rats , indicated by results from fasting-blood glucose , oral glucose tolerance test , fasting insulin levels and histology of pancreas islets .
The @ @ @ @ @ @ @ the down-regulation of PI3K and AKT in liver .
The TUNEL assay analysis of pancreatic tissue showed that HSYA could inhibit the apoptosis of pancreaticβ-cells to a certain extent .
Moreover , HSYA-treatment increased the levels of glycogen synthase and hepatic glycogen and improved lipid metabolism by reducing the triglyceride , total and low-density lipoprotein cholesterol levels , even though it did not change the rats ' body weights .
Conclusion : The results of this study suggested that HSYA could promote PI3K/Akt activation and inhibit the apoptosis of pancreaticβ-cells directly or indirectly @ @ @ @ @ @ @ in HSYA to improve insulin resistance and regulate glycolipid metabolism in T2DM rats .

Background and Aim: Type 2 diabetes mellitus (T2DM), a complex metabolic disease, has become a major public health issue around the world. Hydroxysafflor yellow A (HSYA) is the major active chemical ingredient of. (safflower), which is widely used in patients with cardiovascular and cerebrovascular diseases in China. The aim of this study was to investigate the anti-diabetic effect and potential mechanism of HSYA on the high-fat diet (HFD) and streptozotocin (STZ-)-induced T2DM rats.
Materials and Methods: T2DM rats were induced by feeding HFD (60% fat) for four weeks followed by intraperitoneal injection of a low dose of streptozocin (35mg/kg). The T2DM rats were treated with HSYA (120mg/kg) or metformin (90mg/kg) for eight weeks. Biochemical analysis, histological analysis and Western blot analysis were conducted after 8 weeks of intervention.
Results: The treatment with HSYA evidently reduced fasting-blood glucose and insulin resistance in T2DM rats, indicated by results from fasting-blood glucose, oral glucose tolerance test, fasting insulin levels and histology of pancreas islets. The Western blot results revealed that HSYA reversed the down-regulation of PI3K and AKT in liver. The TUNEL assay analysis of pancreatic tissue showed that HSYA could inhibit the apoptosis of pancreaticβ-cells to a certain extent. Moreover, HSYA-treatment increased the levels of glycogen synthase and hepatic glycogen and improved lipid metabolism by reducing the triglyceride, total and low-density lipoprotein cholesterol levels, even though it did not change the rats' body weights.
Conclusion: The results of this study suggested that HSYA could promote PI3K/Akt activation and inhibit the apoptosis of pancreaticβ-cells directly or indirectly, which might be the underlying mechanisms in HSYA to improve insulin resistance and regulate glycolipid metabolism in T2DM rats.


greenmedinfo--2020-12-16--Safflower yellow improves insulin sensitivity in high-fat diet-induced obesity.

AIMS/INTRODUCTION : Safflower yellow ( SY ) and its main component , hydroxysafflor yellow A , have been demonstrated to show anti-obesity effects .
Peroxisome proliferator-activated receptor-γ2 ( PPARγ2 ) is a critical transcription factor in adipose tissue metabolism .
The aim of the present study was to explore the effects of SY in high-fat diet-induced obese mice , and further investigate the mechanism involving PPARγ2 .
METHODS : High-fat diet-induced obese mice were given 120 mg/kg/day SY for 8 weeks .
Glucose and insulin tolerance tests were carried out .
Fat mass and serum levels of glucose and insulin @ @ @ @ @ @ @ signaling pathway-related genes and PPARγ2 in the adipose tissue was measured .
In vitro , the effects of SY ( 0-500 mg/L ) andhydroxysafflor yellow A ( 0-100 mg/L ) on PPARγ2 promoter activities and PPARγ2 messenger ribonucleic acid ( mRNA ) levels in 3T3-L1 preadipocytes or adipocytes were also detected .
RESULTS : Safflower yellow reduced fat mass , decreased glucose levels and improved insulin sensitivity in obese mice .
SY also increased the mRNA levels of insulin signaling pathway-related genes , and increased PPARγ2 mRNA levels by 39.1 % in subcutaneous @ @ @ @ @ @ @ could reduce fat mass , decrease glucose levels and improve insulin sensitivity in high-fat diet-induced obese mice .
The probable mechanism is to increase PPARγ2 expression by stimulating PPARγ2 promoter activities , further increasing the expression of insulin signaling pathway-related genes in subcutaneous adipose tissue .

AIMS/INTRODUCTION: Safflower yellow (SY) and its main component, hydroxysafflor yellow A, have been demonstrated to show anti-obesity effects. Peroxisome proliferator-activated receptor-γ2 (PPARγ2) is a critical transcription factor in adipose tissue metabolism. The aim of the present study was to explore the effects of SY in high-fat diet-induced obese mice, and further investigate the mechanism involving PPARγ2.
METHODS: High-fat diet-induced obese mice were given 120 mg/kg/day SY for 8 weeks. Glucose and insulin tolerance tests were carried out. Fat mass and serum levels of glucose and insulin were measured. The expression of insulin signaling pathway-related genes and PPARγ2 in the adipose tissue was measured. In vitro, the effects of SY (0-500 mg/L) andhydroxysafflor yellow A (0-100 mg/L) on PPARγ2 promoter activities and PPARγ2 messenger ribonucleic acid (mRNA) levels in 3T3-L1 preadipocytes or adipocytes were also detected.
RESULTS: Safflower yellow reduced fat mass, decreased glucose levels and improved insulin sensitivity in obese mice. SY also increased the mRNA levels of insulin signaling pathway-related genes, and increased PPARγ2 mRNA levels by 39.1% in subcutaneous adipose tissue (P < 0.05). In vitro, SY and hydroxysafflor yellow A significantly enhanced PPARγ2 promoter activities by 1.3-2.1-fold, and increased PPARγ2 mRNA levels by 1.2-1.6-fold in 3T3-L1 preadipocytes or adipocytes (P < 0.05).
CONCLUSIONS: SY could reduce fat mass, decrease glucose levels and improve insulin sensitivity in high-fat diet-induced obese mice. The probable mechanism is to increase PPARγ2 expression by stimulating PPARγ2 promoter activities, further increasing the expression of insulin signaling pathway-related genes in subcutaneous adipose tissue.


greenmedinfo--2020-12-16--Effect and safety of hydroxysafflor yellow A for injection in patients with acute ischemic stroke of

Effect and safety of hydroxysafflor yellow A for injection in patients with acute ischemic stroke of blood stasis syndrome.

OBJECTIVE : To assess the effect and safety of Hydroxysafflor Yellow A for Injection ( HSYAI ) in treating patients with acute ischemic stroke ( AIS ) and blood stasis syndrome ( BSS ) .
METHODS : A multicenter , randomized , double-blind , multiple-dose , active-controlled phase II trial was conducted at 9 centers in China from July 2013 to September 2015 .
Patients with moderate or severe AIS and BSS were randomly assigned to low- , medium- , high-dose HSYAI groups ( 25 , 50 and 70 mg/d HSYAI by intravenous infusion , respectively ) , and a @ @ @ @ @ @ @ , DZXXI ) 30 mL/d by intravenous infusion ) , for 14 consecutive days .
The primary outcome was the Modified Rankin Scale ( mRS ) score⩽1 at days 90 after treatment .
The secondary outcomes included the National Institute of Health Stroke Scale ( NIHSS ) score ⩽1 , Barthel Index ( BI ) score ⩾95 , and BSS score reduced ⩾30 % from baseline at days 14 , 30 , 60 , and 90 after treatment .
The safety outcomes included any adverse events during 90 days after treatment .
RESULTS @ @ @ @ @ @ @ the effectiveness analysis , 66 , 67 , 65 and 68 cases were in the low- , medium- , and high-dose HSYAI and control groups , respectively .
The proportions of patients in the medium- and high-dose HSYAI groups with mRS score⩽1 at days 90 after treatment were significantly larger than the control group ( P < 0.05 ) .
The incidences of favorable outcomes of NIHSS and BI at days 90 after treatment as well as satisfactory improvement of BSS at days 30 and 60 after treatment in the medium- and high-dose @ @ @ @ @ @ @ the control group ( P < 0.05 ) .
No significant difference was reported among the 4 groups in any specific adverse events ( P > 0.05 ) .
CONCLUSIONS : HSYAI was safe and well-tolerated at all doses for treating AIS patients with BSS .
The medium ( 50 mg/d ) or high dose ( 75 mg/d ) might be the optimal dose for a phase III trial .
( Registration No .
ChiCTR-2000029608 ) .

OBJECTIVE: To assess the effect and safety of Hydroxysafflor Yellow A for Injection (HSYAI) in treating patients with acute ischemic stroke (AIS) and blood stasis syndrome (BSS).
METHODS: A multicenter, randomized, double-blind, multiple-dose, active-controlled phase II trial was conducted at 9 centers in China from July 2013 to September 2015. Patients with moderate or severe AIS and BSS were randomly assigned to low-, medium-, high-dose HSYAI groups (25, 50 and 70 mg/d HSYAI by intravenous infusion, respectively), and a control group (Dengzhan Xixin Injection (, DZXXI) 30 mL/d by intravenous infusion), for 14 consecutive days. The primary outcome was the Modified Rankin Scale (mRS) score⩽1 at days 90 after treatment. The secondary outcomes included the National Institute of Health Stroke Scale (NIHSS) score ⩽1, Barthel Index (BI) score ⩾95, and BSS score reduced ⩾30% from baseline at days 14, 30, 60, and 90 after treatment. The safety outcomes included any adverse events during 90 days after treatment.
RESULTS: Of the 266 patients included in the effectiveness analysis, 66, 67, 65 and 68 cases were in the low-, medium-, and high-dose HSYAI and control groups, respectively. The proportions of patients in the medium- and high-dose HSYAI groups with mRS score⩽1 at days 90 after treatment were significantly larger than the control group (P<0.05). The incidences of favorable outcomes of NIHSS and BI at days 90 after treatment as well as satisfactory improvement of BSS at days 30 and 60 after treatment in the medium- and high-dose HSYAI groups were all significantly higher than the control group (P<0.05). No significant difference was reported among the 4 groups in any specific adverse events (P>0.05).
CONCLUSIONS: HSYAI was safe and well-tolerated at all doses for treating AIS patients with BSS. The medium (50 mg/d) or high dose (75 mg/d) might be the optimal dose for a phase III trial. (Registration No. ChiCTR-2000029608).


greenmedinfo--2020-12-16--Safflower yellow and its main component HSYA alleviate diet-induced obesity.

Purpose : Oxidative stress plays an important role in the pathogenesis of obesity and its associated disorders .
Safflower yellow ( SY ) and hydroxysafflor yellow A ( HSYA ) , the natural compounds isolated from , has been found to possess antioxidative and anti-obesity properties .
The purpose of the present study is to investigate whether SY and its main component HSYA alleviate obesity by the antioxidant effects .
Methods : Diet-induced obese ( DIO ) mice were treated with 200 mg/kg/d SY or HSYA for 10 weeks .
Body weight , fat mass , serum biochemical parameters and @ @ @ @ @ @ @ measured .
Glucose and insulin tolerance tests were performed .
The expression of antioxidant enzymes in liver and adipose tissue were measured .
In vitro , HO-induced oxidative stress HepG2 cells and 3T3-L1 adipocytes were treated with SY and HSYA to investigate the direct effects of SY and HSYA on the expression of antioxidant enzymes .
Results : SY and HSYA significantly decreased the body weight gain of DIO mice , and decreased fat mass to 57.8 % and 61.6 % of the control mice , respectively ( < 0.05 ) .
The @ @ @ @ @ @ @ were improved after SY and HSYA treatment .
The hepatic SOD activities and the mRNA levels of antioxidant enzymes in liver and adipose tissue of SY and HSYA treated mice were increased ( < 0.05 ) .
Meanwhile , the administration of SY and HSYA on the HO-induced oxidative stress HepG2 cells and adipocytes also increased the expression of the antioxidant factor and antioxidant enzymes to 1.2~3.3 folds of the control cells ( < 0.05 ) .
Conclusion : SY and its main component HSYA could significantly decrease the fat mass , and @ @ @ @ @ @ @ diet-induced obese mice .
The beneficial effects of SY and HSYA on obesity and metabolism may be associated with the increased expression of antioxidant enzymes in liver and adipose tissue .

Purpose: Oxidative stress plays an important role in the pathogenesis of obesity and its associated disorders. Safflower yellow (SY) and hydroxysafflor yellow A (HSYA), the natural compounds isolated from, has been found to possess antioxidative and anti-obesity properties. The purpose of the present study is to investigate whether SY and its main component HSYA alleviate obesity by the antioxidant effects.
Methods: Diet-induced obese (DIO) mice were treated with 200 mg/kg/d SY or HSYA for 10 weeks. Body weight, fat mass, serum biochemical parameters and superoxide dismutase (SOD) activities were measured. Glucose and insulin tolerance tests were performed. The expression of antioxidant enzymes in liver and adipose tissue were measured. In vitro, HO-induced oxidative stress HepG2 cells and 3T3-L1 adipocytes were treated with SY and HSYA to investigate the direct effects of SY and HSYA on the expression of antioxidant enzymes.
Results: SY and HSYA significantly decreased the body weight gain of DIO mice, and decreased fat mass to 57.8% and 61.6% of the control mice, respectively (<0.05). The parameters of glucose metabolism and liver function were improved after SY and HSYA treatment. The hepatic SOD activities and the mRNA levels of antioxidant enzymes in liver and adipose tissue of SY and HSYA treated mice were increased (<0.05). Meanwhile, the administration of SY and HSYA on the HO-induced oxidative stress HepG2 cells and adipocytes also increased the expression of the antioxidant factor and antioxidant enzymes to 1.2~3.3 folds of the control cells (<0.05).
Conclusion: SY and its main component HSYA could significantly decrease the fat mass, and improve glucose metabolism and liver function in diet-induced obese mice. The beneficial effects of SY and HSYA on obesity and metabolism may be associated with the increased expression of antioxidant enzymes in liver and adipose tissue.


greenmedinfo--2020-12-16--Safflower yellow improves the synaptic structural plasticity.

Safflower yellow ( SY ) is the main effective component of Carthamus tinctorius L. , and Hydroxysafflor yellow A ( @ @ @ @ @ active component with the highest content in SY .
SY and HSYA have been shown @ @ @ @ @ several AD models .
In this study , we aimed to clarify whether the effects @ @ @ @ @ the learning and memory abilities of Aβ-induced AD model rats are related to the enhancement @ @ @ @ @ brain tissues and the amelioration of disorder of glutamate circulation .
We used rats injected @ @ @ @ @ as a model of AD .
After treatment with SY and HSYA , the learning @ @ @ @ @ Aβ-induced AD model rats were enhanced , Aβ deposition in the AD model rats was @ @ @ @ @ dendritic spines and the loss of synaptic-associated proteins were alleviated , and the disorder of @ @ @ @ @ The results indicated that SY and HSYA improve synaptic structural plasticity by ameliorating the disorder @ @ @ @ @ AD model rats .

Safflower yellow (SY) is the main effective component of Carthamus tinctorius L., and Hydroxysafflor yellow A (HSYA) is the single active component with the highest content in SY. SY and HSYA have been shown to have neuroprotective effects in several AD models. In this study, we aimed to clarify whether the effects of SY and HSYA on the learning and memory abilities of Aβ-induced AD model rats are related to the enhancement of synaptic structural plasticity in brain tissues and the amelioration of disorder of glutamate circulation. We used rats injected with Aβinto the bilateral hippocampus as a model of AD. After treatment with SY and HSYA, the learning and memory abilities of the Aβ-induced AD model rats were enhanced, Aβ deposition in the AD model rats was decreased, structural damage to dendritic spines and the loss of synaptic-associated proteins were alleviated, and the disorder of glutamate circulation was ameliorated. The results indicated that SY and HSYA improve synaptic structural plasticity by ameliorating the disorder of glutamate circulation in Aβ-induced AD model rats.


greenmedinfo--2020-12-16--Hepatoprotective effects of hydroxysafflor yellow A in D-galactose-treated aging mice.

Hydroxysafflor yellow A ( HSYA ) is an effective chemical component isolated from Chinese herb Carthamus tinctorius L. In present study , we aimed to evaluate the effects of HSYA on D-galactose- ( D-gal- ) induced aging in mice , and to elucidate the underlying mechanism .
Male C57BL/6 mice were intraperitoneal injection of D-gal and HSYA for 8 weeks .
The body weight gain , spleen and thymus coefficients were determined .
Levels of super dismutase ( SOD ) , catalase ( CAT ) , glutathione peroxidase ( GSH-Px ) and malondialdehyde ( MDA ) in serum and liver @ @ @ @ @ @ @ changes and the SA-β-Gal activity in liver tissues were detected by hematoxylin and eosin and SA-β-Gal staining .
The expression levels of p16 , CDK4 , CDK6 and phosphorylation levels of Retinoblastoma ( Rb ) were detected by immunohistochemistry and western blot analysis .
mRNA levels of genes regulated by p16-Rb pathwaywere determined by quantitative real-time PCR .
In vivo , HSYA improved the aging changes including body weight , organ index and antioxidant status such as activities of SOD , CAT , GSH-Px and MDA in D-gal treated aging mice .
HSYA @ @ @ @ @ @ @ liver tissues induced by D-gal .
Furthermore , HSYA significantly decreased the mRNA and protein level of cyclin-dependent kinase inhibitor p16 , followed by increasing CDK4/6 protein expression and decreasing the phosphorylation of Retinoblastoma ( pRb ) which up-regulated the expression of downstream genes CCNE1 , CCNA2 , P107 and MCM4 .
Collectively , these data indicated that HSYA could ameliorate aging , especially hepatic replicative senescence resulting from D-gal , the mechanism could be associated with the suppression of p16-Rb pathway .

Hydroxysafflor yellow A (HSYA) is an effective chemical component isolated from Chinese herb Carthamus tinctorius L. In present study, we aimed to evaluate the effects of HSYA on D-galactose- (D-gal-) induced aging in mice, and to elucidate the underlying mechanism. Male C57BL/6 mice were intraperitoneal injection of D-gal and HSYA for 8 weeks. The body weight gain, spleen and thymus coefficients were determined. Levels of super dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in serum and liver were measured using commercial kits. Pathological changes and the SA-β-Gal activity in liver tissues were detected by hematoxylin and eosin and SA-β-Gal staining. The expression levels of p16, CDK4, CDK6 and phosphorylation levels of Retinoblastoma (Rb) were detected by immunohistochemistry and western blot analysis. mRNA levels of genes regulated by p16-Rb pathwaywere determined by quantitative real-time PCR. In vivo, HSYA improved the aging changes including body weight, organ index and antioxidant status such as activities of SOD, CAT, GSH-Px and MDA in D-gal treated aging mice. HSYA also dramatically attenuated pathologic changes of aging liver tissues induced by D-gal. Furthermore, HSYA significantly decreased the mRNA and protein level of cyclin-dependent kinase inhibitor p16, followed by increasing CDK4/6 protein expression and decreasing the phosphorylation of Retinoblastoma (pRb) which up-regulated the expression of downstream genes CCNE1, CCNA2, P107 and MCM4. Collectively, these data indicated that HSYA could ameliorate aging, especially hepatic replicative senescence resulting from D-gal, the mechanism could be associated with the suppression of p16-Rb pathway.


greenmedinfo--2020-12-17--Protective effect of hydroxysafflor yellow A on bleomycin- induced pulmonary inflammation and fibros

Protective effect of hydroxysafflor yellow A on bleomycin- induced pulmonary inflammation and fibrosis.

OBJECTIVE : To observe the effect of hydroxysafflor yellow A ( HSYA ) , an active ingredient of a traditional Chinese herbal medicine Carthamus tinctorius L. , on lung inflflammation and pulmonary fibrosis induced by bleomycin ( BLM ) in rats .
METHODS : Animals were divided into 6 groups including normal group , model group , three HSYA groups and dexamethasone ( DXM ) group .
Three doses of HSYA ( 35.6 , 53.3 , and 80.0 mg•kg•day ) were intraperitoneally ( i.p . )
injected in rats for 3 weeks after BLM administration and DXM was used as @ @ @ @ @ @ @ ) .
Arterial blood gas was assayed and morphological changes were observed .
Lung mRNA expressions of tumor necrosis factor ( TNF ) -α , interleukin ( IL ) -1β , IL-6 and some cytokines in lung tissue were detected by real-time polymerase chain reaction .
Nuclear factor-κB p65 or α-smooth muscle actin ( α-SMA ) protein distribution in rat lung tissue was observed by immunohistochemistry .
RESULTS : On the 7th day after BLM administration , lung tissue showed serious inflammation .
Treatment with HSYA or DXM ameliorated lung inflammation .
After @ @ @ @ @ @ @ partial pressure ( PaO ) increased ( HSYA 80.0 mg•kg , P < 0.01 ) and COpartial pressure ( PaCO ) decreased ( HSYA 53.3 , 80.0 mg•kg , P < 0.05 ) .
Moreover , the mRNA expression of TNF-α , IL-1β , and IL-6 ; and the number of NF-κB p65 positive cells was lower in HSYA 53.3 and 80.0 mg•kggroups than those in the model group ( all P < 0.05 ) .
Twenty-one days after BLM administration , HSYA or DXM treatment ameliorated fibrosis , increased PaO2 ( HSYA @ @ @ @ @ @ @ 0.01 ) , and decreased PaCO2 ( 53.3 and 80.0 mg•kg-1 , P < 0.05 ) .
Further , the mRNA expression of TGF-β1 , α-SMA , and collagen I as well as the number of α-SMA positive cells increased in the model group and HSYA can attenuate these changes ( 53.3 , 80.0 mg•kg , P < 0.05 ) .
Hematoxylin and eosin and Masson 's trichrome staining indicated that the fibrosis and collagen deposition were ameliorated in HSYA groups ( 53.3 , 80.0 mg•kg , P < 0.05 ) .
CONCLUSION @ @ @ @ @ @ @ and chronic pulmonary fibrosis induced by BLM in rats .

OBJECTIVE: To observe the effect of hydroxysafflor yellow A (HSYA), an active ingredient of a traditional Chinese herbal medicine Carthamus tinctorius L., on lung inflflammation and pulmonary fibrosis induced by bleomycin (BLM) in rats.
METHODS: Animals were divided into 6 groups including normal group, model group, three HSYA groups and dexamethasone (DXM) group. Three doses of HSYA (35.6, 53.3, and 80.0 mg•kg•day) were intraperitoneally (i.p.) injected in rats for 3 weeks after BLM administration and DXM was used as the positive control (n=8 or 12). Arterial blood gas was assayed and morphological changes were observed. Lung mRNA expressions of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and some cytokines in lung tissue were detected by real-time polymerase chain reaction. Nuclear factor-κB p65 or α-smooth muscle actin (α-SMA) protein distribution in rat lung tissue was observed by immunohistochemistry.
RESULTS: On the 7th day after BLM administration, lung tissue showed serious inflammation. Treatment with HSYA or DXM ameliorated lung inflammation. After treatment with HSYA or DXM, oxygen partial pressure (PaO) increased (HSYA 80.0 mg•kg, P<0.01) and COpartial pressure (PaCO) decreased (HSYA 53.3, 80.0 mg•kg, P<0.05). Moreover, the mRNA expression of TNF-α, IL-1β, and IL-6; and the number of NF-κB p65 positive cells was lower in HSYA 53.3 and 80.0 mg•kggroups than those in the model group (all P<0.05). Twenty-one days after BLM administration, HSYA or DXM treatment ameliorated fibrosis, increased PaO2 (HSYA 53.3, 80.0 mg•kg-1, P<0.01), and decreased PaCO2 (53.3 and 80.0 mg•kg-1, P<0.05). Further, the mRNA expression of TGF-β1, α-SMA, and collagen I as well as the number of α-SMA positive cells increased in the model group and HSYA can attenuate these changes (53.3, 80.0 mg•kg, P<0.05). Hematoxylin and eosin and Masson's trichrome staining indicated that the fibrosis and collagen deposition were ameliorated in HSYA groups (53.3, 80.0 mg•kg, P<0.05).
CONCLUSION: HSYA could alleviate acute lung inflflammation and chronic pulmonary fibrosis induced by BLM in rats.


greenmedinfo--2020-12-17--Danshensu plus hydroxysafflor yellow A could achieve remarkable synergistic neuroprotective effects

Danshensu plus hydroxysafflor yellow A could achieve remarkable synergistic neuroprotective effects on ischemia-reperfusion injury.

Ischemic stroke is a common cerebrovascular disease with substantial morbidity and mortality worldwide .
However , therapeutic options to minimize the cerebral ischemia-reperfusion ( I/R ) injury are limited .
In China , combination of herb Danshen ( ) and Honghua ( ) is effective for stroke treatment in patients but its underlying mechanism requires further investigation .
Our study was conducted to evaluate and explore the synergistic effects of two herb ingredients Danshensu and hydroxysafflor yellow A ( HSYA ) on cerebral ischemia-reperfusion ( I/R ) injury in rats .
Rats were randomly assigned to the following five groups @ @ @ @ @ @ @ Danshensu group , HSYA group , and Danshensu+HSYA group .
Under our experimental conditions , oxygen-glucose deprivation ( OGD ) model was established to determine the synergistic neuroprotective effects of Danshensu and HSYA .
With such methods as neurological deficits scoring , TTC , HE and TUNEL staining , and ELISA detection , the results demonstrated that administration of either Danshensu or HSYA improved neurological defects and alleviated pro-inflammatory and oxidative stress reactions .
Notably , combination of Danshensu and HSYA exerted more effective results than that used alone .
Furthermore , western @ @ @ @ @ @ @ HSYA combination displayed synergistic regulation on TLR4/NF-κB and Nrf2/HO-1 pathways .
Consistently , Danshensu +HSYA group exhibits better neuroprotection in primary neurons with OGD model compared with Danshensu or HSYA group .
Taken together , we found for the first time that Danshensu plus HSYA could achieve remarkable synergistic neuroprotective effects on I/R injury , which is related to the anti-inflammatory and antioxidant pathways .

Ischemic stroke is a common cerebrovascular disease with substantial morbidity and mortality worldwide. However, therapeutic options to minimize the cerebral ischemia-reperfusion (I/R) injury are limited. In China, combination of herb Danshen () and Honghua () is effective for stroke treatment in patients but its underlying mechanism requires further investigation. Our study was conducted to evaluate and explore the synergistic effects of two herb ingredients Danshensu and hydroxysafflor yellow A (HSYA) on cerebral ischemia-reperfusion (I/R) injury in rats. Rats were randomly assigned to the following five groups: sham group, model group, Danshensu group, HSYA group, and Danshensu+HSYA group. Under our experimental conditions, oxygen-glucose deprivation (OGD) model was established to determine the synergistic neuroprotective effects of Danshensu and HSYA. With such methods as neurological deficits scoring, TTC, HE and TUNEL staining, and ELISA detection, the results demonstrated that administration of either Danshensu or HSYA improved neurological defects and alleviated pro-inflammatory and oxidative stress reactions. Notably, combination of Danshensu and HSYA exerted more effective results than that used alone. Furthermore, western blot analysis results showed that Danshensu and HSYA combination displayed synergistic regulation on TLR4/NF-κB and Nrf2/HO-1 pathways. Consistently, Danshensu +HSYA group exhibits better neuroprotection in primary neurons with OGD model compared with Danshensu or HSYA group. Taken together, we found for the first time that Danshensu plus HSYA could achieve remarkable synergistic neuroprotective effects on I/R injury, which is related to the anti-inflammatory and antioxidant pathways.


greenmedinfo--2020-12-17--Seven Tips for Beating Holiday Stress

Seven Tips for Beating Holiday Stress

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greenmedinfo--2020-12-16--Topical application of Hydroxysafflor Yellow A accelerates the wound healing in streptozotocin induc

Topical application of Hydroxysafflor Yellow A accelerates the wound healing in streptozotocin induced T1DM.

To investigate the effects of Hydroxysafflor Yellow A ( HSYA ) , which is derived from safflower , on the proliferation , migration and angiogenesis of cells in vitro and its potential efficacy in vivo when topically applied to a diabetic wound .
Human umbilical vein endothelial cells ( HUVECs ) and mouse macrophage cells ( RAW264.7 ) were used to evaluate angiogenesis and anti-inflammatory activities , respectively .
The influence of HSYA on the wound scratch assay was investigated in keratinocytes .
A splinted excisional wound model in rats with TIDM induced by streptozotocin was used to assess the @ @ @ @ @ @ @ and secretion of vascular growth factors ( VEGF ) as well as transforming growth factor-β1 ( TGF-β1 ) were evaluated by an ELISA assay and histological staining .
The in vitro results showed that HSYA could significantly enhance both the neovascularization of HUVECs and the migration of keratinocytes .
It showed the significant inhibitory effect on nitric oxide production , indicating theanti-inflammatory activity of HSYA .
In vivo , the topical application of HSYA significantly enhanced the wound closure rate , and the time to complete wound closure was 17 days , whereas @ @ @ @ @ @ @ .
Further , treatment with HSYA exhibited significant granulation tissue formation with higher collagen content , re-epithelialization and angiogenesis according to Masson 's trichrome staining evaluation , VEGE and TGF-β1 ELISA measurement .
In conclusion , HSYA application could be considered a promising therapeutic strategy for treating chronic non-healing diabetic foot ulcers .

To investigate the effects of Hydroxysafflor Yellow A (HSYA), which is derived from safflower, on the proliferation, migration and angiogenesis of cells in vitro and its potential efficacy in vivo when topically applied to a diabetic wound. Human umbilical vein endothelial cells (HUVECs) and mouse macrophage cells (RAW264.7) were used to evaluate angiogenesis and anti-inflammatory activities, respectively. The influence of HSYA on the wound scratch assay was investigated in keratinocytes. A splinted excisional wound model in rats with TIDM induced by streptozotocin was used to assess the effects of wound healing. Collagen disposition and secretion of vascular growth factors (VEGF) as well as transforming growth factor-β1 (TGF-β1) were evaluated by an ELISA assay and histological staining. The in vitro results showed that HSYA could significantly enhance both the neovascularization of HUVECs and the migration of keratinocytes. It showed the significant inhibitory effect on nitric oxide production, indicating theanti-inflammatory activity of HSYA. In vivo, the topical application of HSYA significantly enhanced the wound closure rate, and the time to complete wound closure was 17 days, whereas 30 days were needed with PBS treatment. Further, treatment with HSYA exhibited significant granulation tissue formation with higher collagen content, re-epithelialization and angiogenesis according to Masson's trichrome staining evaluation, VEGE and TGF-β1 ELISA measurement. In conclusion, HSYA application could be considered a promising therapeutic strategy for treating chronic non-healing diabetic foot ulcers.


greenmedinfo--2020-12-16--Hydroxysafflor-yellow A induces human gastric carcinoma BGC-823 cell apoptosis.

BACKGROUND Anti-tumor properties of hydroxysafflor-yellow A ( HSYA ) have been recently revealed , as a series of apoptotic factors were confirmed to be regulated by HSYA and associated with peroxisome proliferator-activated receptor Gamma ( PPARγ ) .
In this study , we investigated the cell apoptosis mechanism of HSYA via activated PPARγ signal in human gastric carcinoma cells .
MATERIAL AND METHODS BGC-823 cells were cultured and divided into 5 independent groups : Tumor , HSYA , HSYA+PPARγ inhibitor ( GW9662 ) , and PPARg agonist ( RGZ ) , RGZ+GW9662 .
Cell proliferative activity was measured by MTT @ @ @ @ @ @ @ by flow cytometry .
The nuclear translocation of PPARγ was detected by immunofluorescence staining chemistry , and mRNA levels of PPARγ and caspase-3 were measured by real-time qPCR .
RESULTS Compared to theRGZ group , the HSYA group ( 100 µM ) showed a similar inhibitory effect on the proliferation process of BGC-823 cells , inducing their apoptosis .
As a result , the transition of BGC-823 cells from G0/G1 phase to S phase was blocked .
HSYA was also found to promote the nuclear translocation of PPARγ , leading to increased expression @ @ @ @ @ @ @ effect of HSYA on BGC-823 cells could be further inhibited by PPARγ inhibitor in group GW9662 .
CONCLUSIONS We report the inhibitory effect of HSYA on the proliferation of BGC-823 cells , which results in activating PPARg-dependentcell cycle blocking and cell apoptosis , suggesting that PPARg is a specific type of HSYA that can induce apoptosis of BGC-823 cells .

BACKGROUND Anti-tumor properties of hydroxysafflor-yellow A (HSYA) have been recently revealed, as a series of apoptotic factors were confirmed to be regulated by HSYA and associated with peroxisome proliferator-activated receptor Gamma (PPARγ). In this study, we investigated the cell apoptosis mechanism of HSYA via activated PPARγ signal in human gastric carcinoma cells. MATERIAL AND METHODS BGC-823 cells were cultured and divided into 5 independent groups: Tumor, HSYA, HSYA+PPARγ inhibitor (GW9662), and PPARg agonist (RGZ), RGZ+GW9662. Cell proliferative activity was measured by MTT. Apoptosis and cell cycle were detected by flow cytometry. The nuclear translocation of PPARγ was detected by immunofluorescence staining chemistry, and mRNA levels of PPARγ and caspase-3 were measured by real-time qPCR. RESULTS Compared to theRGZ group, the HSYA group (100 µM) showed a similar inhibitory effect on the proliferation process of BGC-823 cells, inducing their apoptosis. As a result, the transition of BGC-823 cells from G0/G1 phase to S phase was blocked. HSYA was also found to promote the nuclear translocation of PPARγ, leading to increased expression of PPARγ and caspase-3. The regulatory effect of HSYA on BGC-823 cells could be further inhibited by PPARγ inhibitor in group GW9662. CONCLUSIONS We report the inhibitory effect of HSYA on the proliferation of BGC-823 cells, which results in activating PPARg-dependentcell cycle blocking and cell apoptosis, suggesting that PPARg is a specific type of HSYA that can induce apoptosis of BGC-823 cells.


greenmedinfo--2020-12-16--Five Reasons to Eat More Cranberries

Five Reasons to Eat More Cranberries


greenmedinfo--2020-12-16--Hydroxysafflor yellow A attenuates lipopolysaccharide-induced neurotoxicity and neuroinflammation.

Lipopolysaccharide ( LPS ) -induced neuroinflammation triggers and accelerates the pathogenesis of Parkinson 's disease ( PD ) .L.
, a traditional Chinese medicine , has been widely used for the treatment of cerebrovascular disease .
Hydroxysafflor Yellow A ( HSYA ) is an active component of .
The purpose of this study was to investigate whether HSYA could attenuate LPS-induced neurotoxicity and neuroinflammation in primary mesencephalic cultures .
Cell viability was measured by MTT and LDH assays .
The number of tyrosine hydroxylase ( TH ) positive neuron was observed by immunohistochemistry .
NF-κB p65 and iNOS expressions were @ @ @ @ @ @ @ cytokines including IL-1β and TNF-α were determined by ELISA kits .
Nitric oxide ( NO ) content in the culture medium was assayed .
The results showed that HSYA treatment significantly attenuated the LPS-induceddopaminergic neurons damage .
HSYA partially inhibited the expressions of NF-κB p65 and iNOS .
Furthermore , HSYA decreased the content of IL-1β , TNF-α and NO in the supernatants .
Taken together , these results suggest that HSYA exerts protective effects on LPS-induced neurotoxicity in dopaminergicneurons and the mechanisms may be associated with the inhibition of inflammatory response .

Lipopolysaccharide (LPS)-induced neuroinflammation triggers and accelerates the pathogenesis of Parkinson's disease (PD).L., a traditional Chinese medicine, has been widely used for the treatment of cerebrovascular disease. Hydroxysafflor Yellow A (HSYA) is an active component of. The purpose of this study was to investigate whether HSYA could attenuate LPS-induced neurotoxicity and neuroinflammation in primary mesencephalic cultures. Cell viability was measured by MTT and LDH assays. The number of tyrosine hydroxylase (TH) positive neuron was observed by immunohistochemistry. NF-κB p65 and iNOS expressions were evaluated with western blotting method. Pro-inflammatory cytokines including IL-1β and TNF-α were determined by ELISA kits. Nitric oxide (NO) content in the culture medium was assayed. The results showed that HSYA treatment significantly attenuated the LPS-induceddopaminergic neurons damage. HSYA partially inhibited the expressions of NF-κB p65 and iNOS. Furthermore, HSYA decreased the content of IL-1β, TNF-α and NO in the supernatants. Taken together, these results suggest that HSYA exerts protective effects on LPS-induced neurotoxicity in dopaminergicneurons and the mechanisms may be associated with the inhibition of inflammatory response.


greenmedinfo--2020-12-16--[VIDEO] The COVID Vaccine is Here… And so are Potential Side Effects…


greenmedinfo--2020-12-16--[VIDEO] Vaccinated vs. Unvaccinated: The Study the CDC Refused to do -- Interview with Dr. Weiler


greenmedinfo--2020-12-16--Oral hydroxysafflor yellow A reduces obesity in mice by modulating the gut microbiota and serum meta

Oral hydroxysafflor yellow A reduces obesity in mice by modulating the gut microbiota and serum metabolism.

Given the high and increasing prevalence of obesity , the safe and effective treatment of obesity would be beneficial .
@ @ @ @ @ oral hydroxysafflor yellow A ( HSYA ) , an active compound from the dried florets @ @ @ @ @ can reduce high-fat ( HF ) diet-induced obesity in C57BL/6 J mice .
Our results @ @ @ @ @ weight of HF group treated by HSYA was significantly lower than that of the HF @ @ @

Given the high and increasing prevalence of obesity, the safe and effective treatment of obesity would be beneficial. Here, we examined whether oral hydroxysafflor yellow A (HSYA), an active compound from the dried florets of Carthamus tinctorius L., can reduce high-fat (HF) diet-induced obesity in C57BL/6 J mice. Our results showed that the average body weight of HF group treated by HSYA was significantly lower than that of the HF group (P < 0.01). HSYA also reduced fat accumulation, ameliorated insulin resistance, restored glucose homeostasis, reduced inflammation, enhanced intestinal integrity, and increased short-chain fatty acids (SCFAs) production in HF diet-fed mice. Sequencing of 16S rRNA genes in fecal samples demonstrated that HSYA reversed HF diet induced gut microbiota dysbiosis. Particularly, HSYA increased the relative abundances of genera Akkermansia and Romboutsia, as well as SCFAs-producing bacteria, including genera Butyricimonas and Alloprevotella, whereas it decreased the phyla Firmicutes/Bacteroidetes ratioof HF diet-fed mice. Additionally, serum metabolomics analysis revealed that HSYA increased lysophosphatidylcholines (lysoPCs), L-carnitine and sphingomyelin, and decreased phosphatidylcholines in mice fed a HF diet, as compared to HF group. These changed metabolites were mainly linked with the pathways of glycerophospholipid metabolism and sphingolipid metabolism. Spearman's correlation analysis further revealed that Firmicutes was positively while Bacteroidetes and Akkermansia were negatively correlated with body weight, fasting serum glucose and insulin. Moreover, Akkermansia and Butyricimonas had positive correlations with lysoPCs, suggestive of the role of gut microbiota in serum metabolites. Our findings suggest HSYA may be a potential therapeutic drug for obesity and the gut microbiota may be potential territory for targeting of HSYA.


greenmedinfo--2020-12-16--Protective effect of hydroxysafflor yellow A against acute kidney injury.

This study aimed to evaluate the protective effect of hydroxysafflor yellow A ( HSYA ) on ischemia/reperfusion ( I/R ) -induced acute kidney injury via the TLR4/NF-κB pathway , both in vitro and in vivo .
Rats were subjected to removal of the right kidney and I/R injury to the left kidney .
Rats subjected to renal I/R injury were treated with HSYA at 0.5 h prior to I/R injury .
Renal function , histopathological analysis , and cells apoptosis were measured in vivo .
In vitro , proximal renal tubular cells ( HK-2 ) were subjected to hypoxia/reoxygenation ( @ @ @ @ @ @ @ inflammatory cytokines , Toll-like receptor 4 ( TLR4 ) , and nuclear factor ( NF ) -κB expression were determined .
Treatment of I/R rats with HSYA markedly reduced the levels of serum creatinine and blood urea nitrogen , attenuated renal cell apoptosis , alleviated changes in renal tissue morphology , and reduced IL-1β , TNF-α , and caspase-3 release .
In vitro , HSYA effectively decreased NF-κB p65 and inflammatory cytokines , such as IL-1β , TNF-α , and IL-6 .
Thus , HSYA can protect renal function from I/R injury by @ @ @ @ @ @ @ promoting tubular cell survival via the TLR4/NF-κB pathway .
These results suggest that HSYA can be used to prevent I/R-induced acute kidney injury .

This study aimed to evaluate the protective effect of hydroxysafflor yellow A (HSYA) on ischemia/reperfusion (I/R)-induced acute kidney injury via the TLR4/NF-κB pathway, both in vitro and in vivo. Rats were subjected to removal of the right kidney and I/R injury to the left kidney. Rats subjected to renal I/R injury were treated with HSYA at 0.5 h prior to I/R injury. Renal function, histopathological analysis, and cells apoptosis were measured in vivo. In vitro, proximal renal tubular cells (HK-2) were subjected to hypoxia/reoxygenation (H/R). Apoptotic cell death and inflammatory cytokines, Toll-like receptor 4 (TLR4), and nuclear factor (NF)-κB expression were determined. Treatment of I/R rats with HSYA markedly reduced the levels of serum creatinine and blood urea nitrogen, attenuated renal cell apoptosis, alleviated changes in renal tissue morphology, and reduced IL-1β, TNF-α, and caspase-3 release. In vitro, HSYA effectively decreased NF-κB p65 and inflammatory cytokines, such as IL-1β, TNF-α, and IL-6. Thus, HSYA can protect renal function from I/R injury by ameliorating acute kidney injury and partly by promoting tubular cell survival via the TLR4/NF-κB pathway. These results suggest that HSYA can be used to prevent I/R-induced acute kidney injury.


greenmedinfo--2020-12-16--Hydroxysafflor yellow A targets the NF-κB and MAPK pathways and ameliorates the development of osteo

Hydroxysafflor yellow A targets the NF-κB and MAPK pathways and ameliorates the development of osteoarthritis.

The inflammatory environment has been demonstrated to be strongly associated with the progression of osteoarthritis ( OA ) .
HSYA , the main active component in the medical and edible dual purpose plant safflower , has previously showed significant anti-inflammatory effects in several diseases .
In the current study , the protective effects of HSYA in the inhibition of OA development and its underlying mechanism were examined by both in vitro and in vivo experiments .
Our data indicated that interleukin-1 beta ( IL-1β ) induced over-production of pro-inflammatory cytokines , such as nitric oxide ( NO ) and prostaglandin @ @ @ @ @ @ @ the expression of cyclooxygenase-2 ( COX-2 ) , tumor necrosis factor alpha ( TNF-α ) , interleukin-6 ( IL-6 ) and inducible nitric oxide synthase ( iNOS ) were all inhibited by pretreatmentwith HSYA in a dose-dependent manner ( 2.5 to 40 μM ) .
Furthermore , HSYA attenuated IL-1β-induced degradation of the extracellular matrix ( ECM ) by decreasing the expression of metalloproteinases ( MMPs ) and thrombospondin motifs 5 ( ADAMTS5 ) .
Mechanistically , HSYA suppressed IL-1β-induced activationof the nuclear factor kappa B ( NF-κB ) and mitogen-activated protein kinase @ @ @ @ @ @ @ molecular docking studies revealed that HSYA has excellent binding abilities to p65 , extracellular signal-regulated kinase ( ERK ) , p38 and c-Jun N-terminal kinase ( JNK ) .
In addition , the protective effects of HSYA were observed in a surgically induced mouse OA model .
In summary , this study provides evidence that HSYA can be applied as a potential therapeutic agent in the treatment of OA .

The inflammatory environment has been demonstrated to be strongly associated with the progression of osteoarthritis (OA). HSYA, the main active component in the medical and edible dual purpose plant safflower, has previously showed significant anti-inflammatory effects in several diseases. In the current study, the protective effects of HSYA in the inhibition of OA development and its underlying mechanism were examined by both in vitro and in vivo experiments. Our data indicated that interleukin-1 beta (IL-1β) induced over-production of pro-inflammatory cytokines, such as nitric oxide (NO) and prostaglandin E2 (PGE2); also, the expression of cyclooxygenase-2 (COX-2), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and inducible nitric oxide synthase (iNOS) were all inhibited by pretreatmentwith HSYA in a dose-dependent manner (2.5 to 40 μM). Furthermore, HSYA attenuated IL-1β-induced degradation of the extracellular matrix (ECM) by decreasing the expression of metalloproteinases (MMPs) and thrombospondin motifs 5 (ADAMTS5). Mechanistically, HSYA suppressed IL-1β-induced activationof the nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) cascades. Meanwhile, molecular docking studies revealed that HSYA has excellent binding abilities to p65, extracellular signal-regulated kinase (ERK), p38 and c-Jun N-terminal kinase (JNK). In addition, the protective effects of HSYA were observed in a surgically induced mouse OA model. In summary, this study provides evidence that HSYA can be applied as a potential therapeutic agent in the treatment of OA.


greenmedinfo--2020-12-16--Hydroxysafflor yellow A protects against angiotensin II‑induced hypertrophy.

Myocardial infarction ( MI ) is life‑threatening and is generally accompanied by myocardial hypertrophy .
Notably , Hydroxysafflor yellow A ( HSYA ) can prevent tissue injuries .
The objective of this study was to investigate the effect of HSYA on hypertrophy after MI .
Hematoxylin and eosin ( H & E ) staining assays were performed to measure cell area .
The protein synthesis rate was assessed using the 3H Leucine incorporation assay .
Reverse transcription‑quantitative polymerase chain reaction ( RT‑qPCR ) , western blot analysis and the immunohistochemical assay were used to detect the expression of target genes @ @ @ @ @ @ @ SOD ) , malondialdehyde ( MDA ) and the reactive oxygen species ( ROS ) generation were examined using commercial kits .
Decreased myocardial hypertrophy was observed in animals treated with HSYA .
Furthermore , the expression of nuclear factor ( erythroid‑derived 2 ) ‑like 2 ( Nrf2 ) was higher in HSYA administration groups compared with that in the MI model group .
In H9c2 cardiomyocytes , the pretreatmentwith HSYA increased the cell viability , however , it reduced protein synthesis rate , mitigated cell surface area and decreased the expression of @ @ @ @ @ @ @ β‑myosin heavy chain ( β‑MHC ) .
By contrast , the downregulation of Nrf2 deteriorated and reversed the effect of Ang II and HSYA .
Furthermore , oxidative stress was alleviated by HSYA via inhibiting ROS generation , modulating the activities of SOD and MDA .
In addition , the expression of NAD ( P ) H : quinone oxidoreductase 1 ( NQO1 ) and heme oxygenase‑1 ( HO‑1 ) were recovered by the pretreatment of HSYA that was combated by siNrf2 .
In conclusion , HSYA exerted anti‑hypertrophic effects , which was @ @ @ @ @ @ @ pathway .
The findings of this study may inspire a novel strategy to combat MI .

Myocardial infarction (MI) is life‑threatening and is generally accompanied by myocardial hypertrophy. Notably, Hydroxysafflor yellow A (HSYA) can prevent tissue injuries. The objective of this study was to investigate the effect of HSYA on hypertrophy after MI. Hematoxylin and eosin (H&E) staining assays were performed to measure cell area. The protein synthesis rate was assessed using the 3H Leucine incorporation assay. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), western blot analysis and the immunohistochemical assay were used to detect the expression of target genes. The activity of superoxide dismutase (SOD), malondialdehyde (MDA) and the reactive oxygen species (ROS) generation were examined using commercial kits. Decreased myocardial hypertrophy was observed in animals treated with HSYA. Furthermore, the expression of nuclear factor (erythroid‑derived 2)‑like 2 (Nrf2) was higher in HSYA administration groups compared with that in the MI model group. In H9c2 cardiomyocytes, the pretreatmentwith HSYA increased the cell viability, however, it reduced protein synthesis rate, mitigated cell surface area and decreased the expression of Brain natriuretic factor (BNP) and β‑myosin heavy chain (β‑MHC). By contrast, the downregulation of Nrf2 deteriorated and reversed the effect of Ang II and HSYA. Furthermore, oxidative stress was alleviated by HSYA via inhibiting ROS generation, modulating the activities of SOD and MDA. In addition, the expression of NAD(P)H:quinone oxidoreductase 1 (NQO1) and heme oxygenase‑1 (HO‑1) were recovered by the pretreatment of HSYA that was combated by siNrf2. In conclusion, HSYA exerted anti‑hypertrophic effects, which was pertinent with the activation of Nrf2/NQO‑1/HO‑1 signaling pathway. The findings of this study may inspire a novel strategy to combat MI.