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目的 研究尼古丁对心肌细胞H9C2的影响及其机制.方法 将培养的H9C2细胞分为4组即对照组、尼古丁组(10 μmol/L)、对照+丝苏氨酸蛋白激酶(Akt)过表达组、尼古丁(10 μmol/L) +Akt过表达组.孵育48 h后用细胞增殖与毒性检测试剂盒(CCK-8)检测细胞活性率;Caspase活性检测试剂盒检测凋亡率;Western blot法检测Akt蛋白表达水平.结果 与对照组相比,尼古丁组细胞活性明显降低(P＜0.05),细胞凋亡显著升高(P＜0.01),Akt蛋白水平显著下调(P＜0.01).Akt过表达可有效改善尼古丁引起的细胞活性的降低(P＜0.01)减少细胞凋亡.结论 尼古丁通过下调Akt蛋白表达水平引起心肌细胞的凋亡.“,”AIM To determine the effect of nicotine on cardiomyocytes and the mechanism underlying it.METHODS Cultured H9C2 cells were randomly divided into 4 groups:control group,nicotine group(10 μmol/L),control + Akt overexpression group and nicotine (10 μmol/L) + Akt overexpression group.Forty-eight hours after culture,cell viability was detected by CCK-8,apoptosis was detected by Caspase-3 colorimetric activity assay kit and the protein level of Akt was detected by Western blot.RESULTS Compared with the control group,the cell viability of the nicotine group was obviously decreased(P ＜0.05),the cell apoptosis was remarkably improved (P ＜ 0.01) and the protein level of Akt was decreased (P ＜ 0.01).These changes were all reversed by Akt overexpression (P ＜ 0.01).CONCLUSION Nicotine down-regulates the protein level of Akt,which can induce the apoptosis of H9C2 cells.