【摘要】 目的观察G蛋白偶联雌激素受体（GPER）对过氧化氢（H₂O₂）诱导的H9C2心肌细胞凋亡的影响,并探讨其机制。方法培养H9C2心肌细胞,按随机数表法分组,给予0.2 mmol/L H₂O₂或0.2 mmol/L H₂O₂及不同浓度的GPER特异性激动剂G-1（1、10、100μmol/L）。采用流式细胞仪检测细胞凋亡;Westernblot法检测细胞中JNK信号通路及Bcl-2家族、caspase-3相关蛋白表达。结果心肌细胞经不同浓度G-1预处理后,H₂O₂诱导的心肌细胞凋亡率均明显下降,p-JNK、Bax蛋白、caspase-3蛋白表达明显降低,Bcl-2表达明显增高（均P<0.05）。结论 G-1可能通过抑制Bcl-2和JNK信号通路,减轻H₂O₂诱导的H9C2心肌细胞凋亡。更多还原

【Abstract】 Objective To investigate the effect of G protein-coupled estrogen receptor（GPER） on the apoptosis of cardiomyocytes induced by hydrogen peroxide（H₂O₂） and to explore its possible mechanism.Methods H9 C2 cardiomyocytes were randomly divided into 0.2 mmol/L H₂O₂ or 0.2 mmol/L H₂O₂ with different concentrations of GPER specific agonists G-1（1, 10, 100 μmol/L）. Cell apoptosis was detected by flow cytometry. JNK signaling pathway and Bcl-2 family and caspase-3 related protein expression in cardiac myocytes were detected by Westernblot.Results After pretreatment with different concentrations of G-1,the apoptosis of cardiomyocytes induced by H₂O₂ decreased significantly,the expression of p-JNK, Bax and caspase-3 decreased significantly, and the expression of Bcl-2 increased significantly（all P<0.05）.Conclusion G-1 may alleviated H₂O₂ induced cardiomyocyte apoptosis partly by inhibiting Bcl-2 and JNK signaling pathways.更多还原