目的 探讨缝隙连接蛋白Cx43是否参与硫化氢后处理减轻离体大鼠心脏缺血/再灌注(I/R)损伤.方法 72只♂SD大鼠随机分为6组(n=12):空白组(Sham组),缺血/再灌注组 (I/R组),溶媒组 (DMSO 组),抑制剂18β-次甘草酸组(AGA组),硫化氢后处理组 (NP 组),硫化氢后处理+AGA组 (N+A组).采用离体心脏 Langendorff灌注模型,平衡灌注 20 min后,停灌 30 min,复灌 60 min.记录平衡末及灌注结束时的心率 (HR)、左室舒张末期压 (LVEDP)、左室发展压 (LVDP)、左室内压上升最大速率(+dp/dtmax)、左室内压下降最大速率(-dp/dtmax);灌注结束时,TTC染色法检测心肌梗死面积;Western blot半定量线粒体和胞质总的Cx43(total connexin 43,tCx43)和磷酸化Cx43(phosphorylated connexin 43,pCx43)表达水平.结果 平衡灌注末各组间心功能指标差异无统计学意义.再灌注后,与I/R组比较,NP组明显改善再灌注损伤心功能的各项指标(P 0. 05 ). After reperfusion, compared with I/R group, NP group had better hemodynamics , the myocardial infarct size was much lower( P < 0. 05 ), the expression of tCx43 in mitochondria increased significantly , but decreased significantly in cytosol, the expression of pCx43 was same to tCx43. However, 18β-AGA abolished the cardioprotective effects offered by hydrogen sulfide postconditioning and decreased tCx43 and pCx43 expression in mitochondria( P <0. 05 ). Conclusion Exogenous hydrogen sulfide postconditioning effectively protects isolated rat hearts against ischemia and reperfusion injury via activating Cx43.
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