【摘要】 目的:探讨咪达唑仑对缺氧复氧损伤所致大鼠心肌细胞凋亡的影响及与外周型苯二氮卓类受体(PBR)的关系。方法:将培养融合的心肌细胞随机分为7组,即对照组(C组)、缺氧复氧组(HR组)、PK11195组(P组)、Ro5-4864组(R组)、咪达唑仑组(M组)、PK11195+Ro5-4864组(PR组)和PK11195+咪达唑仑组(PM组)。建立缺氧复氧损伤模型。流式细胞仪检测细胞凋亡。结果:PR组细胞凋亡,与R组比较差异显著(P<0.01),与HR组比较无显著差异。M组细胞凋亡,与HR组比较差异显著(P<0.05)。PM组细胞凋亡与M组比较无显著差异。PR组PBRmRNA表达,与R组比较差异显著(P<0.01),与HR组比较无显著差异。M组、PM组、HR组PBRmRNA表达比较无显著差异。结论:激活PBR明显抑制缺氧复氧所致的大鼠心肌细胞凋亡。咪达唑仑减轻缺氧复氧引起的心肌细胞凋亡,其作用是非PBR依赖性的。更多还原

【Abstract】 Objective:To investigate the effect of midazolam on cardiac myocyte apoptosis induced by hypoxia/reoxygenation and its relationship with peripheral benzodiazepine receptor (PBR). Methods:The cardiac myocytes were divided into 7 groups:group C (control group),group HR (hypoxia/reoxygenation group),group P,group R,group M,group PR,and group PM. The cardiomyocytes were treated with PK11195 (a PBR antagonist) in group P,Ro5-4864 (a PBR agonist) in group R,midazolam in group M,PK11195 plus Ro5-4864 in group PR,and PK11195 plus midazolam in group PM,respectively. The cardiac myocyte apoptosis was determined by flow cytometer. Results:There was significant difference in the apoptosis rate of cardiac myocyte between groups PR and R and between groups M and HR (P < 0.01,P < 0.05). No significant difference was found in the apoptosis rate of cardiac myocyte between groups PR and HR and between groups PM and M. There was significant difference in the PBR mRNA expression between groups PR and R (P < 0.01). No significant difference was found in the PBR mRNA expression between groups PR and HR. Conclusion:The activation of PRB significantly inhibits the cardiac myocyte apoptosis induced by hypoxia/reoxygenation. Midazolam could prevent the cardiac myocyte apoptosis induced by hypoxia/reoxygenation in a PBR-independent manner.更多还原