论文部分内容阅读
为探讨γ -IFN、NO在实验性病毒性心肌炎小鼠中的变化及其在病毒性心肌炎中的作用 ,以柯萨奇病毒B3亲心肌株(CVB3m)诱导的BALB/C心肌炎小鼠为研究对象 ,每隔7天观察小鼠血清中γ -IFN、心肌匀浆中NO在病程中的动态变化 ,并计算感染小鼠心肌组织光镜下病理积分。结果显示 ,BALB/C鼠感染病毒后体内γ -IFN、NO均有不同程度升高 ,急性期(第7天)最高 ,且NO的升高与γ -IFN相关(r=0.95,r2=0.9,P<0.05) ,而感染后心肌病理积分又与NO相关(r=0.66,r2=0.43,P<0.05)。结果表明 ,γ -IFN在病毒性心肌炎发病中起重要作用 ,介导NO产生以发挥抗病毒作用 ,而过分表达则可造成自身损伤 ,故适当降低其表达水平有利于病理转归
To investigate the changes of γ-IFN and NO in experimental viral myocarditis in mice and their roles in viral myocarditis, we investigated the effects of coxsackievirus B3 (CVB3m) on BALB / c myocarditis in mice Subjects were observed every 7 days in mice serum γ-IFN, myocardial homogenate NO in the course of the course of the dynamic changes, and calculate the pathological score of infected mice myocardial tissue under light microscopy. The results showed that the expression of IFN-γ and NO in BALB / c mice increased to different extents, the highest in the acute phase (day 7), and the increase of NO was correlated with γ-IFN (r = 0.95, r2 = 0.9 , P <0.05). The pathological scores of myocardium after infection were also correlated with NO (r = 0.66, r2 = 0.43, P <0.05). The results showed that γ-IFN played an important role in the pathogenesis of viral myocarditis, mediated the production of NO to play an antiviral effect, and overexpression could cause self-injury, so properly reducing the expression level is conducive to pathological outcome