摘要
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 role of calcium-sensing receptor （CaR） on isebemia/ reperfusion-induced rat cardiomyocyte apoptosis. Methods The isolated rat hearts were subjected to 40 rain iscbemia followed by 2b of reperfusion with or without CaR agonist GdCls at the beginning of reperfusion. Control hearts （without iscbemia） and iscbemic bearts （40 min iscbemia without reperfusion） served as controls. The protein expressions of CaR, Bcl-2 and cyt C were detected by Western blot. Cardiomyocyte apoptosis was detected by TUNEL Mitocbondrial potential （△Фm ） was detected by laser confocal microscopy. Results Compared to controls groups, the expressions of CaB. and apoptotic cells were significantly increased, △Фm and expressions of mitochondria cyt C and Bcl-2 were significantly reduced in ischemia/reporfusion hearts with or without C, dCls. Conclusion CaB. was involved in the induction of cardiomyocyte apoptosis during ischemia/reperfusion via mitochondrial pathway.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
2007年第8期740-744,共5页
Chinese Journal of Cardiology
基金
国家自然科学基金(30370577)
哈尔滨医科大学青年基金项目(060015)
