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目的探讨高糖应激早期对H9c2细胞存活的影响及其可能的信号转导通路。方法高糖培养H9c2细胞24 h后,收集细胞进行细胞活力和凋亡的测定,用Western blot方法测定蛋白激酶(Akt)的磷酸化水平和内皮细胞一氧化氮合酶(eNOS)的表达。结果与对照(NG)组相比,高糖培养(HG)组H9c2细胞活力改善,凋亡减少,而PI3K抑制剂LY294002预处理和NOS抑制剂L-NAME预处理均抑制短期高糖培养对H9c2细胞的保护作用。与NG组相比,HG组早期Akt磷酸化水平升高,eNOS蛋白表达增加,结论在高糖应激早期(24 h内),高糖通过活化PI3K/Akt/eNOS信号通路,改善H9c2细胞的活力,减少其凋亡。
Objective To investigate the effect of high glucose stress on the survival of H9c2 cells and its possible signal transduction pathway. Methods H9c2 cells were cultured with high glucose for 24 h. The viability and apoptosis of cells were measured. The phosphorylation of Akt and the expression of eNOS in endothelial cells were detected by Western blot. Results Compared with the control group, H9c2 cells in high glucose (HG) group showed a decrease in cell viability and apoptosis, whereas both PI3K inhibitor LY294002 and NOS inhibitor L-NAME inhibited the growth of H9c2 cells Cell protection. Compared with NG group, the phosphorylation of Akt increased and the expression of eNOS protein increased in the early stage of HG group. Conclusion High glucose can improve the expression of H9c2 cells by activating PI3K / Akt / eNOS signal pathway in the early stage of high glucose stress Vitality, reduce its apoptosis.