【摘要】 探讨牛磺酸对高糖诱导H9c2心肌细胞凋亡的影响及其作用机制,以H9c2心肌细胞,分3组:正常对照组(CN组,葡萄糖浓度为5.5 mmol·L^-1)、高糖组（HG组,葡萄糖浓度为25.5 mmol·L）、牛磺酸干预组(TAU组,葡萄糖浓度为25.5mmol·L^-1基础上加终浓度为40 mmol·L^-1牛磺酸)。48 h后,采用MTT检测心肌细胞活力,荧光酶标仪检测胞内ROS含量,RT-PCR法检测PI3KmRNA表达量,ELISA法检测磷酸化Akt蛋白（phospho-Akt,p-Akt）蛋白含量,比色法检测Caspase3水平,并采用Annexin-V/PI结合流式细胞仪检测细胞凋亡率。结果:高糖诱导48 h后细胞活力下降（P<0.001）,ROS含量升高（P<0.001）,PI3KmRNA水平与p-Akt蛋白含量降低（P<0.001）,Caspase3活性升高（P<0.001）;并伴有凋亡率显著增加（P<0.001）;与HG组相比,牛磺酸干预可显著提高细胞活力（P<0.001）,降低ROS含量（P<0.001）,增加PI3KmRNA表达（P<0.01）与p-Akt蛋白含量（P<0.05）,降低Caspase3活性（P<0.001）,抑制细胞凋亡（P<0.001）。说明牛磺酸可通过PI3K/Akt途径降低细胞内氧化应激水平和Caspase3活性,抑制高糖诱导H9c2心肌细胞的凋亡。更多还原

【Abstract】 To investigate the effects and mechanisms of taurine on H9c2 cell apoptosis induced by high glucose,H9c2 cells cultured in vitro were divided into three groups:CN group(5.5 mmol·L^-1glucose),HG group(25.5 mmol·L^-1glucose) and TAU group(25.5 mmol·L^-1glucose and 40 mmol·L^-1taurine).After 48 h,the cell activity was detected by MTT;Intracellular ROS levels were detected with microplate readers;Levels of PI3 KmRNA and phospho-Akt were respectively detected with RT-PCR and ELISA.The activity of Caspase3 was measured with enzyme-linked colorimetry assay and Annexin V/PI double marking method was used to detect cell apoptosis.High glucose on H9c2 cells can significantly reduce the cell activity（P < 0.001）,levels of PI3KmRNA（P < 0.001） and p-Akt（P < 0.001）,and increase the level of intracellular ROS（P < 0.001）,activity of Caspase3（P < 0.001） and ratio of cell apoptosis（P < 0.001）.Compared with the HG group,taurine intervention can increase the cell activity（P < 0.001）,levels of PI3KmRNA（P < 0.01） and p-Akt（P < 0.05）,and remarkablely decrease the level of intracellular ROS（P < 0.001）,activity of Caspase3（P < 0.001） and ratio of cell apoptosis（P < 0.001）.It is conclued that taurine inhibits the H9c2 cell apoptosis from oxidative stress induced by high glucose,through the PI3K/Akt signaling pathway.更多还原