NF-κB途径在病毒性心肌炎小鼠中的作用

Role of NF-κB Pathway in Viral Myocarditis Mice

目的探讨NF-κB途径在病毒性心肌炎(VMC)小鼠发病中的作用。方法将60只小鼠按随机数字表法分为对照组20只与模型组40只,模型组小鼠腹腔注射0.1mL嗜心性柯萨奇B3病毒Nancy株(CVB3)病毒悬液;对照组腹腔注射0.1mL Eagle’S培养液。取对照组与模型组造模后4、10d心脏组织,采用HE染色观察2组心肌病理改变情况,定量RT-PCR检测2组心肌NF-κB mRNA表达水平;Western blot检测2组心肌NF-κB及磷酸化的IκB(p-IκB)蛋白表达水平。结果对照组心肌细胞未见异常;模型组造模后4d心肌细胞出现坏死,有炎性细胞浸润,造模后10d心肌细胞发生巨大病变,有大量炎性细胞感染。模型组造模后4、10dNF-κB mRNA及NF-κB、p-IκB蛋白的表达水平均显著高于对照组(P<0.05),而模型组造模后10d较造模后4d又显著升高(P<0.05)。结论 CVB3病毒通过NF-κB途径诱导小鼠心肌产生炎性反应。

Objective To investigate the role of NF-κB pathway in the pathogenesis of viral myocarditis（VMC）mice.Methods Sixty mice were intraperitoneally injected with either 0.1mLCoxsackievirus B3（CVB3）suspension（model group,n=40）or 0.1mL Eagle＇s medium（control group,n=20）.Cardiac tissues were collected 4and 10 days after injection,and myocardial pathological changes were observed by HEstaining.The expression of NF-κB mRNA in myocardium was measured by RT-PCR,and the expression of NF-κB and phospho-IκB（p-IκB）protein was measured by Western blot.Results In control group,no abnormalities were found in myocardial cells.However,myocardial cellnecrosis and inflammatory cell infiltration were observed in model group 4days after CVB3 injection.Furthermore,severemyocardial lesions and a large number of inflammatory cells were observed in model group 10 days after CVB3 injection.Compared with control group,the expression of NF-κB mRNA,NF-κB protein and p-IκB protein significantly increased in model group in a time-dependentmanner（P〈0.05）.Conclusion CVB3 induces inflammatory responsethrough NF-κB pathway in VMC mice.