巨噬细胞炎性蛋白-1α在小鼠病毒性心肌炎中的表达  

Expression of macrophage inflammatory protein 1α in mice with viral myocarditis

作　　者：陈静[1] 范晓晨[1] 

机构地区：[1]安徽医科大学第一附属医院儿科,安徽合肥230022

出　　处：《临床儿科杂志》2013年第10期964-967,共4页Journal of Clinical Pediatrics

基　　金：安徽省自然科学基金资助项目(No.2009ZY36)

摘　　要：目的探讨病毒性心肌炎(VMC)小鼠巨噬细胞炎性蛋白-1α(MIP-1α)的动态变化和作用。方法 120只雄性4周龄BALB/c小鼠随机分为VMC组80只,对照组40只。VMC组小鼠腹腔接种柯萨奇B3病毒建立VMC模型,对照组接种不含病毒DMEM液。接种后第3、7、15、30天每组各取10只处死,留取心脏标本,用免疫组织化学技术检测心肌MIP-1α蛋白表达水平,HE染色检查心脏病理变化,分析MIP-1α水平与心肌病变程度的相关性。结果 VMC组小鼠接种病毒后第3天心肌组织MIP-1α蛋白表达水平开始升高,第7天达高峰,此后逐渐下降,至第30天仍维持在较高水平。在各时间点,VMC组小鼠的MIP-1α水平均高于对照组,差异有统计学意义(P<0.05),且与心肌病理学积分呈显著正相关(r=0.94,P<0.01)。结论 MIP-1α过度表达可能在VMC的发病机制中起重要作用。Objective To detect the expression of macrophage inflammatory protein la （MIP-la） in the myocardium of viral myoearditis （VMC） mice at different phases. Methods A total of 120 4-week-old male BALB/c mice were randomly divided into 2 groups, 80 in the VMC group and 40 in the control group. Mice in VMC group were inoculated intraperitoneally with coxsackievirus B3 to build VMC models, while mice in control group were treated with DMEM cultivate liquid. Ten mice of each group were sacrificed on days 3, 7, 15 and 30 after treatment and their heart tissues were collected for analysis. The level of MIP-la in the myocardium was determined by immunohistochemistry. Myocardial histopathology was examined with hematoxylin and eosin stain. In addition, the relationship between the level of MIP-1α and the degree of myocardial lesion was investigated. Results The expression of myocardial MIP-la protein in VMC group was up-regulated in myocardium on day 3 after inoculation of virus, and slowly decreased after the peak on day 7, but still sustained a high level on day 30. Compared with the control group, the levels of MIP-la in VMC group were increased significantly at every phase （P〈0.05）. Furthermore, positive correlation was found between MIP-la protein expression levels and myocardial histopathologic scores in VMC group （r=0.94, P〈0.01）. Conclusion The up-regulated expression of MIP-1α may play a critical role in the pathogenic mechanisms of viral myocarditis.

关 键 词：趋化因子CCL3 心肌炎 免疫组织化学 小鼠 

分 类 号：R725.4[医药卫生—儿科]