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目的 探讨Fas/Fasl介导的细胞凋亡在病毒性心肌炎(VM)小鼠发病中的作用。方法 采用光镜观察小鼠心肌组织病理改变;电镜技术、原位末端标记法(TUNEL)检测细胞凋亡;免疫组化技术检测不同时期Fas、Fasl蛋白表达。结果 感染后7～10d凋亡细胞数及Fas、Fasl蛋白表达水平逐渐升高,心肌病变以炎症细胞浸润及心肌坏死为主并逐渐加重,10～14d细胞凋亡及Fas、Fasl蛋白表达水平最高,心肌病变也最重,21～28d细胞凋亡数及Fas、Fasl蛋白表达水平逐渐下降,心肌炎症细胞浸润及坏死逐渐减轻,代之以成纤维细胞增生及心肌纤维化;Fasl蛋白表达与心肌病变积分呈显著正相关(r=0.86 P<0.01)。结论Fas/Fasl介导的细胞凋亡是VM心肌损伤的机制之一;Fas、Fasl基因在VM细胞凋亡中起重要作用。
Objective To investigate the role of Fas / Fasl-mediated apoptosis in the pathogenesis of viral myocarditis (VM) in mice. Methods The pathological changes of myocardium were observed by light microscopy. The apoptosis was detected by electron microscopy and TUNEL. The expressions of Fas and Fasl protein were detected by immunohistochemistry. Results The number of apoptotic cells and the expressions of Fas and Fasl proteins gradually increased from 7th to 10th day after infection. The main pathological changes were inflammatory cell infiltration and myocardial necrosis. The apoptosis and the expression of Fas and Fasl protein tended to be the highest on the 10th ~ 14th day , Myocardial lesions also the heaviest, 21 ~ 28d apoptotic cells and Fas, Fasl protein expression levels gradually decreased myocardial inflammatory cell infiltration and necrosis gradually reduced, replaced by fibroblasts and myocardial fibrosis; Fasl protein expression and myocardial Lesion score was positively correlated (r = 0.86 P <0.01). Conclusion Fas / Fasl-mediated apoptosis is one of the mechanisms of VM myocardial injury. Fas and Fasl genes play an important role in VM apoptosis.