小鼠病毒性心肌炎细胞凋亡相关蛋白的表达

目的 探讨嗜鼠心肌Ｃｏｘｓａｃｋｉｅ Ｂ３病毒（ＣＶＢ３ｍ）诱导的ＢＡＬＢ／Ｃ小鼠病毒性心肌炎（ＶＭＣ）细胞凋亡的机制。方法 给ＢＡＬＢ／Ｃ小鼠腹腔接种０．１ｍｌ１００ＴＣＤ５０ＣＶＢ３ｍ，感染后批断脊处死小鼠，应用双重荧光染色技术、原位末端标记法（ＴＵＮＥＬ）和共聚焦显微镜对小鼠心肌细胞凋亡及部分相关蛋白表达进行检测。结果 ＣＶＢ３ｍ可诱发小鼠ＶＭＣ。感染病毒后９～１２ｄ病变达到高峰，检出率达１

Expression of apoptosis related proteins perforin,granzyme B and caspase-8 in experimental viral myocarditis of mice

Objective To explore the mechanisms of apoptosis in mice myocaditis induced by CVB_ 3m .Methods BALB/C mice were inoculated with 0.1ml 100 TCD_ 50 CVB_ 3m and batch sacrificed later.Histologic,immunohistochemical observations including TUNEL labeling method,and dual fluorescent labeling techniques were performed on mice hearts,and the results were detected by a confocal laser scanning microscopy.Results The myocarditis were detected from all 100% CVB_ 3m infected mice and were most severe at 7~12 days.Apoptosis also increased markedly in inflammatory cells and myocyted at 9~15 days after infection.Immunoreactivities for perforin,granzyme B,caspase-8 and Bax increased considerably in myocardium after infection,and decreased gradually after 20 days,as inflammation subsided.No significant differences were observed in hearts of infected mouse as compared to controls for Bcl-2.Double staining for Bax demonstrated apoptosis in some inflammatory cells.Conclusions The perforin and granzyme B take part in the regulation of myocyte damage and apoptosis in mice myocarditis.Our data suggest that increases of reaction of Caspase-8 and Bax/Bcl-2 was related to apoptosis.