柯萨奇B2病毒致低硒乳鼠心肌细胞凋亡及其调控的实验研究

Experimental study on characteristics of suckling mouse myocardium apoptosis and regulating mechanism induced by Se-deficiency and infection of Coxsackie B2 virus

目的 观察低硒条件下野毒株柯萨奇B2病毒(CVB2)感染对乳鼠心肌细胞凋亡的影响及调控。方法 应用低硒合成饲料(含硒0.016 mg／kg)喂养昆明鼠5周后交配,取其子代7日龄乳鼠经腹腔注入107TCID50CVB2 0.1 ml,9 d后处死,取其心脏。TUNEL法检测心肌细胞凋亡的发生情况,免疫组化方法对凋亡相关基因蛋白的表达情况进行检测。结果 补硒病毒组和低硒对照组乳鼠心肌均可检测到凋亡细胞,而补硒对照组和低硒病毒组未见细胞凋亡发生。各组乳鼠C-myc、Bcl-2、p53以及TGFβ-1蛋白表达异常。结论 低硒和病毒分别作用均可引起乳鼠心肌细胞发生凋亡。低硒条件下感染CVB2(野毒株)不能引起心肌细胞发生凋亡。

Objective To observe the effects of Coxsackie B2 virus(CVB2) and selenium dificiency on suckling mouse myocardium apoptosis and discuss the regulating mechanism. Methods Kunming mice were fed with synthetic diet which is deficient in selenium (level of selenium = 0.016 mg/kg), and were mated after 5 week. Their suckling mice were injected with 107 TCID50 CVB2 0.1 ml introperitoneally on day 7 after birth, and on day 9 after injection the suckling mice were killed and their hearts were taken out. The cardiocyte apoptosis was detected by TUNEL, and the expression of the proteins associated with apoptosis was examined. Results In the selenium-adequate and virus-infected group and the selenium-deficient group myocadical apoptosis was observed,but neither in the selenium-adequate group nor in the selenium-deficient and virus-infected group. In mice of various groups, C-myc, Bcl-2, p53, and TGFβ-1 proteins expressed abnormally. Conclusions Selenium-deficient and virus could induce the cardiocyte apoptosis of the suckling mice separately, but selenium-deficiency infection of CVB2 could not induce the cardiocyte apoptosis.