PI3K/AKT通路在刺五加保护大鼠缺血再灌注心肌细胞损伤中的作用

目的研究刺五加注射液对缺血再灌注损伤心肌细胞的保护作用机制中PI3K/AKT信号通路的作用。方法取Wistar大鼠幼鼠心室肌细胞进行体外培养,缺氧及复氧各3h建立缺血再灌注损伤细胞模型。培养的心肌细胞分成:正常对照组(Co),缺血再灌注组(I/R),I/R+复方刺五加注射液组(Pi)和I/R+复方刺五加注射液+LY294002(Pi+Ly)。采用免疫细胞化学染色法和Western-bloting检测细胞内P-AKT蛋白含量。结果免疫细胞化学染色法及Western-bloting结果均显示,IR组P-AKT蛋白表达水平明显高于正常对照组;实验组(Pi)与其他各组(IR、Pi+Ly)比较,实验组(Pi)P-AKT蛋白表达水平明显升高(P0.05)。结论刺五加注射液减轻心肌缺血再灌注损伤可能与其激活PI3K/AKT信号通路有关。

The effect of PI3K/AKT signaling pathway on myocardial ischemia-reperfusion by acanthopanax injection

Objective To study the protective mechanism of acanthopanax injection on myocardial cells with ischemia-reperfusion injury. Methods Newborn Wistar rats hearts were isolated and cardiomyocytes were separated by trypsin digestion. The primary cardiomyocytes were collected and incubated in vitro.Ischemia- reperfusion injury model was established by 3 hours of hypoxia and 3 hours of reoxygenation subsequently. The cultured cardiomyocytes were divided into： normal control（Co）, ischemic reperfuson（I/R）, I/R＋ acanthopanax（Pi）and Pi＋LY294002（Pi＋Ly） groups.The levels of P-AKT protein were detected by immunocytochemistry and Western-bloting. Results Immunocytochemical and Western-blotting results showed that the expression levels of P-AKT in the cultured cardiomyocytes were significantly increased in I/R group than in Co group, and also increased in the Pi group compared with the I/R or Pi＋Ly groups（ P〈0.05）. Conclusion Reduction of myocardial ischemia-reperfusion injury by acanthopanax injection might be related to the activation of the PI3K/AKT signaling pathway.