黄芪皂苷IV对LPS诱导大鼠心肌损伤的保护作用及机制

Protective Effect and Mechanism of Astragaloside IV on LPS-induced Cardiomyocyte Injury

目的:研究黄芪皂苷IV对LPS诱导的大鼠心肌损伤的保护作用及机制。方法:心肌细胞的活力,乳酸脱氢酶(LDH)的释放,肌酸激酶(CK)的含量被测量来判断心肌细胞损伤的程度。对超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、肿瘤坏死因子-α(TNF-α)的释放以及Sirt1的蛋白表达进行评估。结果:1,3和10μM黄芪皂苷IV可显著降低LPS诱导的心肌细胞LDH,CK和MDA的生成;黄芪皂苷IV可剂量依赖性地增加SOD的活性,减少TNF-α的释放。黄芪皂苷IV的干预可剂量依赖性的增加由LPS刺激而引起的乳鼠心肌细胞Sirt1蛋白的表达。结论:结果表明,黄芪皂苷IV可通过调控氧化应激和Sirt1-TNF-α途径有效发挥对LPS诱导大鼠心肌损伤的保护作用。

Objective： To investigate the effect and mechanisms of Astragaloside IV on LPS-induced cultured neonatal rat cardiomyoeyte injury. Methods： The viability, the release of lactate dehydrogenase （LDH） and the content of creatine kinase （CK） were selected to evaluate the degree of cardiomyocytes injury. Superoxide dismutase （SOD） activity, malondialdehyde （MDA）, TNF-α, as well as the expression of Sirtl protein were assessed. Results： 1, 3 and 10 μM Astragaloside IV protected LPS-induced rat cardiomyocytes fi＇om injury and significantly decreased LDH release, CK and MDA production. Furthermore, Astragaloside IV increased SOD activity and reduced the release of TNF-α in a concentration-dependent manner. Astragaloside IV increased the expression of Sirtl protein induced by LPS. Conclusion： Astragaloside IV protects cardiac myocytes against LPS-induced injury through cellular oxidative stress and regulating the expression of Sirtl.