摘要
目的探讨Akt在过氧化氢(H2O2)诱导的心肌细胞肥大中的作用。方法用10μmol/L或50μmol/L浓度H2O2处理原代培养的新生大鼠心肌细胞,以细胞体积和蛋白含量反映心肌细胞肥大程度,观察Akt抑制剂对H2O2致心肌细胞肥大的作用;Western blot检测H2O2对Akt的激活效应。结果10μmol/L或50μmol/L的H2O2培养心肌细胞48 h后,细胞体积增大和蛋白含量增高;应用Akt抑制剂后减弱了H2O2刺激心肌细胞肥大的效应;H2O2使心肌细胞Akt磷酸化水平增高,磷脂酰肌醇3-激酶(PI3K)抑制剂Wortmannin和LY294002抑制了H2O2引起的Akt的活化。结论Akt信号通路可能介导了低浓度H2O2所致的心肌细胞肥大。
Objective To investigate the effect of Akt on cardiomyocyte hypertrophy induced by hydrogen peroxide （H2O2）. Methods The neonatal rat cardiomyocytes cultured in primary generation were treated with low concentrations of H2O2. The cardiomyocyte hypertrophy was evaluated by the determination of average cell volume and protein content. The effects of Akt inhibitor on cardiomyocyte hypertrophy induced by H2O2 was recorded. Western blot was performed to examine the phosphorylation of Akt induced by H2O2. ResultsH202 at 10 or 50 μmol/L stimulated cardiomyocyte enlargement as measured by cell volume and the protein content per cell. The inhibitor of Akt inhibited the hypertrophic response of cardiomyoctes stimulated byH2O2. H2O2 increased the level of Akt phosphorylation in cardiomyocytes, while that is suppressed by the inhibitors of PI3K（ phosphoinositide 3-kinase）. Conclusion Akt signaling is involved in cardiomyocyte hypertrophy induced by H2O2.
出处
《基础医学与临床》
CSCD
北大核心
2008年第2期149-152,共4页
Basic and Clinical Medicine
