柯萨奇病毒B4''致低硒鼠心肌损伤及细胞凋亡机制的研究

目的 为了探讨柯萨奇病毒B4’致低硒鼠心肌损伤及细胞凋亡的机理。方法 用低硒和补硒饲料分别喂养昆明鼠，4周后交配，给其子代4周雄性鼠腹腔接种10—7TCID50柯萨奇病毒B4’0．1ml，对照组接种等量RPMI1640培养掖。7天后处死，取心脏制片，光镜观察病变，并采用TUNEL法和免疫组化法技术检测凋亡细胞及其相关基因。结果 低硒和补硒饲料病毒组的心肌病变检出率分别为78．1％和16．7％。低硒和补硒饲料对照组的心肌未见病变。低硒和补硒病毒组及低硒对照组的心肌均发生不同程度的细胞凋亡。补硒对照组未见心肌细胞凋亡。结论 柯萨奇病毒B4’感染低硒昆明鼠引起的心肌损伤有细胞凋亡机制参与。

Experimental research on myocardial injury and mechanism

Objective To investigate the mechanism of Se-deficient mice's myocardial injury and apoptosis induced by CVB4'.Methods The original Kunming mice were fed with Se-supplemented feed and Se-deficient feed respectively and mated after four weeks.The four-week male mice were inoculated intraperitoneally with CVB4',while control group were inoculated with equal-quantity RPMI 1 640 in the same way.Myocardial changes of mice in four groups were observed through light microscope,and the four-week mice's hearts were collected as experimental materials to examine apoptosis and it's related gene expression by using TUNEL and immunohistochemistry methods.Results The detection rate of myocardial lesion in Se-deficient virus group was 78.1%,and that of Se-supplemented virus group was 16.7%.The myocardium of the Se-deficient and Se-supplemented groups had no pathological changes.The myocardium of the Se-deficient virus group,Se supplemented virus group and Se-deficient groups had all apoptosis in different degree.There was no apoptosis in the rich selenium mice's myocardium.Conclusion Myocardial mechanism of apoptosis was involved in myocardial injury induced by CVB4' in Se-deficiency Kunming mice.