细胞凋亡在小鼠病毒性心肌炎中的作用

目的 :探讨柯萨奇病毒 B3(CVB3)所致小鼠病毒性心肌炎 (VM)心肌细胞损伤的变化 ,观察细胞凋亡在心肌损伤中的作用。方法 :采用 CVB3制备小鼠病毒性心肌炎动物模型 ,分别于腹腔接种 CVB3后第 5、7、10、14、2 1、2 8d,取心肌组织切片 HE染色了解心肌损伤 (坏死 )情况 ;电镜和流式细胞仪检测 ,观察心肌中的细胞凋亡。结果 :心肌坏死方面 :光镜观察见对照组小鼠心肌组织无异常改变 ,实验组病鼠可见心肌细胞坏死和单核、淋巴细胞浸润 ,后期可见纤维化 ;心肌细胞凋亡方面 :电镜观察对照组心肌中未检出凋亡细胞 ,而病鼠心肌凋亡细胞检出率较高 5 8.33% (7/12例 ) ,且细胞凋亡多存在于炎症病灶周围的心肌细胞及病灶处炎性浸润细胞 ;各期病鼠心肌组织中的细胞凋亡比率较对照组明显增加 ,流式细胞仪检测平均心肌细胞凋亡百分率为 2 6 .74± 15 .2 2 % ,感染后第 7～ 14 d心肌细胞凋亡百分率明显高于其余时间 (P<0 .0 0 1)。结论 :小鼠病毒性心肌炎中心肌损伤坏死与凋亡共存 ,其中异常的心肌细胞凋亡与病毒性心肌炎的发病过程有关

Apoptosis in Murine Acute Myocarditis Caused by Coxsackievirus B3

Objective:The mechanisms responsible for myocardial injury and cell death in myocarditis are still unclear. In this study, we examined that myocardial cell death occurs in murine acute myocarditis caused by Coxsackie virus B 3 (CVB 3) and whether myocytes apoptosis plays a role in the development of virus myocarditis(VM).Methods:One hundred and thirty BALB/c mice were included in the experiment. Fifteen mice in experimental group inoculated with CVB 3 and five mice in control group injected with Eagle's minimum essential medium (MEM) were sacrificed 5, 7, 10, 14, 21, 28 days post-inoculation (p.i.). Light microscopy, electronic microscopy and flow cytometry (FCM) were used to detect the inflammation, necrosis and apoptosis in myocardium.Results:(1) The typical myocardial lesions including myocardial necrosis and lymphocyte infiltration at the 5th day p.i. were observed, much more obvious at the 7th to 14th day, and recovered gradually from the 21th to 28th day p.i. without any inflammation in control group.(2) Apoptosis myocytes were seen in seven of twelve myocarditis mice by electronic microscopy. Apoptosis cells including myocytes (around the nidus) and infiltrating lymphocytes were detected in the myocardium of myocarditis mice by electronic microscopy. But apoptosis cells were not observed in the mice of control group. (3) The detection rate of apoptosis cells in myocardium was much higher in mice with VM than that in control group.The percent of apoptosis cells increased significantly after the infection 7 to 14 days than 5 p.i.and 21 to 28 days p.i.Conclusion:These findings suggest that cell death via necrosis and apoptosis existed in murine acute myocarditis caused by CVB3 at the same time. Apoptosis of cardiomyocytes and lymphocytes is one of the mechanisms of myocardial injury in VM, and it might play a role in the development of VM.