Sheng Mai San protects H9C2 cells against hyperglycemia-induced apoptosis

被引:4
作者
Pang, Bing [1 ]
Shi, Li-Wei [1 ]
Du, Li-Juan [1 ]
Li, Yun-Chu [1 ]
Zhang, Mei-Zhen [1 ]
Ni, Qing [1 ]
机构
[1] China Acad Chinese Med Sci, Dept Endocrinol, Guanganmen Hosp, 6 Floors Inpatients Bldg,5 Beixiange St, Beijing, Peoples R China
来源
BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE | 2019年 / 19卷 / 01期
基金
中国国家自然科学基金;
关键词
Sheng Mai San; Apoptosis; Bcl-2; Bax signaling way; Fas; FasL signaling way; DIABETIC CARDIOMYOPATHY; OXIDATIVE STRESS; HEART-FAILURE; P53; INHIBITION; MYOCARDIUM; ACTIVATION; MECHANISMS; INJURY; DEATH;
D O I
10.1186/s12906-019-2694-2
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
Background Sheng Mai San (SMS) has been proven to exhibit cardio-protective effects. This study aimed to explore the molecular mechanisms of SMS on hyperglycaemia (HG)-induced apoptosis in H9C2 cells. Methods HG-induced H9C2 cells were established as the experimental model, and then treated with SMS at 25, 50, and 100 mu g/mL. H9C2 cell viability and apoptosis were quantified using MTT and Annexin V-FITC assays, respectively. Furthermore, Bcl-2/Bax signalling pathway protein expression and Fas and FasL gene expression levels were quantified using western blotting and RT-PCR, respectively. Results SMS treatments at 25, 50, 100 mu g/mL significantly improved H9C2 cell viability and inhibited H9C2 cell apoptosis (p < 0.05). Compared to the HG group, SMS treatment at 25, 50, and 100 mu g/mL significantly downregulated p53 and Bax expression and upregulated Bcl-2 expression (p < 0.05). Moreover, SMS treatment at 100 mu g/mL significantly downregulated Fas and FasL expression level (p < 0.05) when compared to the HG group. Conclusion SMS protects H9C2 cells from HG-induced apoptosis probably by downregulating p53 expression and upregulating the Bcl-2/Bax ratio. It may also be associated with the inhibition of the Fas/FasL signalling pathway.
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页数:10
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