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目的 探讨M3受体激动对H2 O2 诱导的大鼠培养心肌细胞凋亡的作用 ,进一步阐明其机制。方法 末端标记法 (TUNEL)进行细胞凋亡检测 ;免疫组化方法检测Bcl 2和Fas的表达 ;共聚焦显微镜观察 [Ca2 + ]i荧光强度变化。结果 M3受体激动剂胆碱 (10mmol·L- 1 )可减少H2 O2 诱导的心肌细胞凋亡的数量 ,并可增加心肌Bcl 2的表达 ,减少Fas表达 ,抑制H2 O2 诱导的 [Ca2 + ]i荧光强度的升高。但预先应用 4DAMP (10nmol·L- 1 )阻断M3受体可逆转胆碱作用。结论 激动M3受体对H2 O2 诱导的心肌细胞凋亡有保护作用 ,其机制可能与Bcl 2和Fas表达以及下调[Ca2 + ]i有关。
Objective To investigate the effect of M3 receptor agonist on H2O2-induced cardiomyocyte apoptosis in rats and to elucidate its mechanism. Methods Cell apoptosis was detected by TUNEL method. The expression of Bcl - 2 and Fas was detected by immunohistochemistry. The fluorescence intensity of [Ca2 +] i was observed by confocal microscopy. Results The M3 receptor agonist choline (10 mmol·L -1) decreased the number of H2O2-induced cardiomyocyte apoptosis, increased the expression of Bcl 2, decreased the expression of Fas, and inhibited the [Ca 2+] i fluorescence intensity increased. But pretreatment with 4DAMP (10nmol·L-1) block M3 receptors can reverse the role of choline. Conclusions Agonist M3 receptor has a protective effect on H2O2-induced cardiomyocyte apoptosis, and its mechanism may be related to the expression of Bcl-2 and Fas and the down-regulation of [Ca2 +] i.