CVB3m病毒致低硒低维生素E鼠心肌损伤的发病机制

目的 为深入研究CVB3m病毒感染导致的低Se低VE鼠心肌病变中氧化损伤的作用。方法 1周龄乳鼠给予低Se低VE饲料喂养，4周后腹腔接种病毒，7d后处死，测定全血谷胱甘肽过氧化物酶（GSH－Px)活性以及肝脏中脂质过氧化物（LPO）含量，光镜下观察心肌的病理改变。结果 Se和VE联合缺乏鼠感染CVB3m病毒7d后，小鼠全血GSH－Px活性下降，肝脏中LPO水平增加，光镜下小鼠心肌病变检出率和严重程度均高于补Se常VE病毒组。结论 氧化应激损伤在病毒性心肌炎实验动物模型的发病机制中起重要作用。

The effect of oxidative stress on myocardial injury induced by CVB3m in Se and VE deficient mice

Objective To study the effect of oxidative stress on myocardial injury induced by CVB3m in Se and VE deficent mice.Methods Feeding the 7-day-old Kunming mice with both Se and VE deficient composite feed for 4 weeks,then inoculating them intraperitoneally with CVB3m,1 week later,killing them by cervical dislocation.The myocardial lesions were observed under light microscope and the activity of GSH-Px of whole blood and the content of LPO in liver were measured.Results Contrasted with the mice fed normally,the mice fed with composite feed demonstrated severe lesions and high morbidity in heart,low GSH-Px activity in blood and high LPO contenti in liver after virus infection.Conclusion Oxidative stress played an important role in myocardial injury induced by CVB3m infection.