scholarly journals Astragaloside IV alleviates heart failure by promoting angiogenesis through the JAK-STAT3 pathway

2019 ◽  
Vol 57 (1) ◽  
pp. 48-54 ◽  
Author(s):  
Yan-Bo Sui ◽  
Yu Wang ◽  
Li Liu ◽  
Feng Liu ◽  
Yi-Qing Zhang
2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Zhiwei Dong ◽  
Pei Zhao ◽  
Ming Xu ◽  
Chen Zhang ◽  
Wei Guo ◽  
...  

2020 ◽  
Vol 58 (1) ◽  
pp. 1192-1198
Author(s):  
Yan-Bo Sui ◽  
Kui-Kui Zhang ◽  
Yu-kun Ren ◽  
Li Liu ◽  
Yan Liu

2021 ◽  
Vol 22 (4) ◽  
Author(s):  
Juan Liu ◽  
Ya Li ◽  
Xiyun Bian ◽  
Na Xue ◽  
Jiancai Yu ◽  
...  

2021 ◽  
Vol 9 (18) ◽  
pp. 1435-1435
Author(s):  
Bei Li ◽  
Junjian Yu ◽  
Peipei Liu ◽  
Taohui Zeng ◽  
Xueliang Zeng

2020 ◽  
Vol 126 ◽  
pp. 110012 ◽  
Author(s):  
Yibei Zang ◽  
Jingjing Wan ◽  
Zhen Zhang ◽  
Si Huang ◽  
Xia Liu ◽  
...  

2021 ◽  
Vol 15 ◽  
Author(s):  
ZhengHu Xu ◽  
Dongfeng Yang ◽  
Xiaojing Huang ◽  
Huai Huang

ObjectivesAstragaloside IV (AS-IV), the main active component of Astragalus membranaceus, bears anti-inflammatory, antioxidant, and neuroprotective activity. Parkinson’s disease (PD) is a common neurodegenerative disease. This study explored the protective effect of AS-IV on the cell model of PD.Materials and MethodsSH-SY5Y cells were incubated with different concentrations (10, 50, 100, 150, and 200 μM) of 6-hydroxydopamine (6-OHDA) for 0, 3, 6, 12, 24, and 48 h to establish the PD cell model. Different concentrations (0, 25, 50, 100, 150, and 200 μM) of AS-IV or 15 mM JAK2/STAT3 pathway inhibitor SC99 was added for intervention 2 h before 6-OHDA treatment. The viability and morphological damage of 6-OHDA-treated SH-SY5Y cells were measured using MTT assay and Hoechst 33258 staining. The expression of microtubule associated protein 2 (MAP2) was detected by immunofluorescence staining. The levels of inflammation and oxidative stress were measured using ELISA. Apoptosis of 6-OHDA-treated SH-SY5Y cells was detected using flow cytometry, and phosphorylation level of JAK2 and STAT3 were detected using Western blot analysis.ResultsThe survival rate of SH-SY5Y cells treated with 100 μM 6-OHDA for 24 h was about 50%. AS-IV (25–100 μM) significantly improved the viability (all p < 0.01), increased MAP2 expression, and repaired the morphological damage induced by 6-OHDA. AS-IV inhibited IL-1β, IL-6, and TNF-α level (all p < 0.05), reduced MDA and ROS content and increased SOD concentration, thereby reducing inflammation and oxidative stress (all p < 0.01) in 6-OHDA-treated SH-SY5Y cells. Moreover, AS-IV decreased apoptosis rate and Bax/Bcl-2 ratio induced by 6-OHDA (all p < 0.05). Mechanically, AS-IV significantly increased the phosphorylation of JAK2 and STAT3 (p < 0.01); the addition of SC99 decreased the cell viability, increased the apoptosis rate, enhanced the levels of inflammatory factors and oxidative stress.ConclusionAS-IV enhanced the cell viability, and inhibited apoptosis, inflammation and oxidative stress of 6-OHDA-treated SH-SY5Y cells via activating the JAK2/STAT3 signaling pathway. This study may confer novel insights for the management of PD.


2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Bin Tang ◽  
Jin-Guo Zhang ◽  
Hong-Yong Tan ◽  
Xi-Qing Wei

Chronic heart failure (CHF) is the end-stage of many cardiovascular diseases and severely affects the patients’ lifespan. Inhibiting ventricular remodeling is thus a primary treatment target for CHF patients. Astragaloside IV (AS-IV) can improve cardiac function and protect myocardial cells. The study aims to investigate the effects of AS-IV on ventricular remodeling and explore its role in regulating energy metabolism using a rat CHF model. Sprague–Dawley rats were divided into five groups (n=20 per group): CHF + benazepril hydrochloride (Benazepril HCL), CHF + low-dose (30 mg.kg−1.day−1) AS-IV, CHF + high-dose (60 mg.kg−1.day−1) AS-IV, and a sham control group. After 8 weeks of treatment, the cardiac structure and functional parameters were measured. Morphological changes in the myocardial tissue in five groups were evaluated. Protein and mRNA expression of peroxisome proliferator-activated receptor α (PPARα), medium-chain acyl-CoA dehydrogenase (MCAD), and muscle carnitine palmitoyl transferase-1 (MCPT1) were also analyzed. Our results showed that the left ventricular mass index (LVMI), collagen volume fraction (CVF), and free fatty acid (FFA) concentration of CHF group rats increased when compared with sham control group, while the protein and mRNA expressions of PPARα, MCAD, and MCPT1 decreased in CHF. Importantly, treatment with AS-IV (CHF + AS-IV group) showed improved heart function and structure, increased expression of PPARα, MCAD, and MCPT1 and improved FFA utilization in comparison with CHF group. In conclusion, our study shows that AS-IV inhibits ventricular remodeling, improves cardiac function, and decreases FFA concentration of CHF model rats. Our findings suggest a therapeutic potential of using AS-IV in CHF.


2009 ◽  
Vol 4 (1) ◽  
pp. 6 ◽  
Author(s):  
Zhuanyou Zhao ◽  
Weiting Wang ◽  
Fang Wang ◽  
Kerui Zhao ◽  
Yingmei Han ◽  
...  

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Wen-Xiao Feng ◽  
Jie Yang ◽  
Yan Li ◽  
Hai-Yan Sun ◽  
Juan Zhang ◽  
...  

Author(s):  
George Hug ◽  
William K. Schubert

A white boy six months of age was hospitalized with respiratory distress and congestive heart failure. Control of the heart failure was achieved but marked cardiomegaly, moderate hepatomegaly, and minimal muscular weakness persisted.At birth a chest x-ray had been taken because of rapid breathing and jaundice and showed the heart to be of normal size. Clinical studies included: EKG which showed biventricular hypertrophy, needle liver biopsy which showed toxic hepatitis, and cardiac catheterization which showed no obstruction to left ventricular outflow. Liver and muscle biopsies revealed no biochemical or histological evidence of type II glycogexiosis (Pompe's disease). At thoracotomy, 14 milligrams of left ventricular muscle were removed. Total phosphorylase activity in the biopsy specimen was normal by biochemical analysis as was the degree of phosphorylase activation. By light microscopy, vacuoles and fine granules were seen in practically all myocardial fibers. The fibers were not hypertrophic. The endocardium was not thickened excluding endocardial fibroelastosis. Based on these findings, the diagnosis of idiopathic non-obstructive cardiomyopathy was made.


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