目的:探讨毛蕊异黄酮(calycosin)抗缺糖缺氧H9c2细胞的保护作用,并初步研究其可能的作用机制。方法:H9c2心肌细胞分为正常对照组、模型组和毛蕊异黄酮处理组,建立缺糖缺氧模型,在H9c2细胞缺糖缺氧前用毛蕊异黄酮预处理2小时,测定培养液中乳酸脱氢酶(LDH)释放量,应用MTT法检测心肌细胞存活率,Western blot检测毛蕊异黄酮对PI3K/Akt和Nrf-2/HO-1信号通路相关蛋白表达的影响。结果:经1-10μM/L的毛蕊异黄酮预处理后,细胞的LDH释放水平显著下降,细胞的存活率高于模型组。毛蕊异黄酮(10μM/L)处理细胞2个小时后,磷酸化Akt/PI3K,Nrf1,Nrf-2,HO-1的蛋白表达升高。结论:毛蕊异黄酮对H9c2细胞的缺糖缺氧诱导细胞损伤有保护效果,其作用可能与激活PI3K/Akt和Nrf2/HO-1信号通路有关。
Objective: To observe the protective effects of calycosin on oxygen glucose deprivation( OGD)-induced cell injury and explore the underlying mechanisms in H9c2 cells. Methods: H9c2 cardiomyocytes were divided into control group,model group,calycosin treated group.OGD-induced model was established. H9c2 cells were exposure OGD condition after pretreatment by calycosin. The cytoprotective effects of calycosin were evaluated by Lactate dehydrogenase( LDH) MTT assays. Western blot analysis was used to determine the expression levels of Akt / PI3 K,Nrf1,Nrf-2,HO-1 to explore the underlying mechanisms of its action. Results: Compared with the normal control group,Pretreatment with calycosin( 1 ~ 10 μM) significantly decreased LDH leakage caused by OGD( P 〈 0. 05),while the cell viability was slightly increased in a concentration dependent manner. The results of Western blot shown that calycosin at the concentration of 10 μM increased the physphorylation of Akt and PI3 K as well as the contents of Nrf1,Nrf-2 and HO-1. Conclusion: Our results demonstrated that calycosin displayed cardioprotective effects against OGD-induced cell injury in H9c2 cells. The underlying mechnisms of its action maybe involve in the activation of PI3 K / Akt and Nrf2 / HO-1 pathways.