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目的探讨钙敏感受体(CaR)参与心肌缺血/再灌注损伤诱发细胞凋亡的机制。方法Langendorff 离体灌流的方法复制心脏缺血/再灌注模型。观察缺血/再灌注和加入 CaR 激动剂时 CaR的表达情况。TUNEL 染色观察不同组别细胞凋亡,应用激光扫描共聚焦显微镜观察大鼠心肌细胞的线粒体膜电位的变化。Western blot 检测心肌组织线粒体中细胞色素 C 及 Bcl-2的表达。结果心肌缺血/再灌注和加入 CaR 激动剂时 CaR 的表达明显高于对照组(P 均<0.01)。TUNEL 染色发现缺血/再灌注组和激动剂组细胞凋亡率明显增加(P 均<0.05),同时此两组的线粒体膜电位下降明显(P 均<0.05),线粒体细胞色素 C 与 Bcl-2的表达也明显下降(P 均<0.05)。结论 CaR 激活在缺血/再灌注时通过诱发线粒体损伤,促进细胞凋亡。
Objective To investigate the mechanism of calcium sensitive receptor (CaR) involved in myocardial apoptosis induced by myocardial ischemia / reperfusion injury. Methods Langendorff was used to replicate cardiac ischemia / reperfusion model by perfusion. To observe the expression of CaR in ischemia / reperfusion and adding CaR agonist. TUNEL staining was used to observe the apoptosis of different groups. Laser scanning confocal microscopy was used to observe the change of mitochondrial membrane potential in rat cardiac myocytes. Western blot was used to detect the expression of cytochrome C and Bcl-2 in myocardial mitochondria. Results The expression of CaR in myocardial ischemia / reperfusion and CaR agonist group was significantly higher than that in control group (all P <0.01). TUNEL staining showed that the apoptosis rate of ischemia / reperfusion group and agonist group were significantly increased (all P <0.05), and the mitochondrial membrane potential of both groups decreased significantly (all P <0.05), mitochondrial cytochrome C and Bcl- 2 expression was also significantly decreased (P all <0.05). Conclusion CaR activates mitochondrial damage and promotes apoptosis during ischemia / reperfusion.