柯萨奇B3病毒感染小鼠心肌硫氧还蛋白的表达

Thioredoxin expression in myocardium of mice infected by Coxsackie virus B3

目的研究硫氧还蛋白(thioredoxin,Trx)在柯萨奇B3病毒感染小鼠心肌炎模型中表达的变化,探讨Trx在病毒性心肌损伤中的作用。方法建立柯萨奇B3病毒感染鼠心肌炎模型,采用光镜检测心肌形态改变,应用RT鄄PCR技术比较接种病毒后不同时间点(7,14,21d)TrxmRNA表达变化。结果7d时心肌病损严重;14d时部分心肌病损开始修复;21d时心肌修复较完全。接种病毒后21d时,硫氧还蛋白mRNA表达与对照组比较明显上调(P<0.01),7d和14d时同对照组相比表达无显著性差异(P>0.05)。结论在急性柯萨奇B3病毒性心肌炎中,Trx可能被急性炎症刺激素特异地诱导,在疾病的后期TrxmRNA表达上调,促进心肌修复,提示适当剂量的Trx可能对急性柯萨奇B3病毒性心肌炎有潜在治疗作用。

Objective To investigate the changes of thioredoxin expression in myocarditis model of mice infected by Coxsackie virus B3 (Nancy strain) for exploring the possible involvement of thioredoxin in the pathogenesis of viral myocarditis. Methods Coxsackie virus B3 myocarditis model was induced in mice. At 7, 14 and 21days post infection, microscopic examination was performed to examine morphological changes of myocardium. Moreover, thioredoxin mRNA expression level was examined with RT-PCR. Results On the 7th day, microscopic examination showed serious myocardial lesions; on the 14th day, parts of the lesions began to improve and on the 21st day, lesions improved thoroughly. On the 21st day, upregulation of thioredoxin mRNA was observed(P < 0.01), but on the 7th and the 14th day, no such result was found(P > 0.05). Conclusions In acute Coxsackie virus B3 myocarditis, thioredoxin might be specifically induced by acute inflammatory stimuli and upregulated in the late stage. It contributes to the improvement of myocardial lesions. Appropriate dosage of thioredoxin might have potential therapeutical effect on the improvement of Coxsackie virus B3 myocarditis.