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目的 研究病毒性心肌炎(VMC)小鼠心肌组织趋化因子(ChKs)表达谱表化,探讨ChKs在VMC发病中的可能作用及意义。方法 B3型柯萨奇病毒(CVB3)腹腔注射雄性BALB/c小鼠;RT-PCR定性和实时定量分析心肌组织MCP-1、IP-10.Ltn和FKN第12种ChKs表达。病理切片和血清CK-MB分析判定病变和病损程度。结果 (1)在所检测的12种ChKs中,VMC组呈阳性表达的有9种,显著多于正常组心肌组织的6种,有3种ChKs(BLC.Eot和LARC)两组均未检出;(2)VMC组9种阳性表达的ChKs中CVB3诱导性表达的为MIP-2、MIG和IP-10.6种组成性表达的ChKs在VMC时上调表达的有MIP-1β、MCP-1、MCP-2.Ltn等4种,下调表达的有RANTES,与正常对照相比未呈现明显差异的为FKN。(3)ChKs的表达消长存在一定的差异,感染4 d后MIP-2等达高峰,随后下降;9 d后出现MCP-1和RANTES表达上升峰;FKN在感染9 d内表达较稳定。(4)亚急性早期、中期、中后期和晚期心肌组织ChKs表达谱有明显区别,各期ChKs表达谱中优势表达的ChKs分别为IP-10、IP-10、MPC-1、MCP-1。结论 VMC心肌组织ChKs呈成簇性方式改变,表达谱改变的复杂性可能与发病机制的复杂性有关,优势表达的ChKs可能在病毒性心肌炎发病中扮演着更重要的角色。
Objective To investigate the expression of chemokine (ChKs) in myocardium of viral myocarditis (VMC) mice and to explore the possible role and significance of ChKs in the pathogenesis of VMC. Methods Male BALB / c mice were inoculated intraperitoneally with CVB3 B3. The expression of 12th ChKs in myocardium MCP-1, IP-10.Ltn and FKN were analyzed by RT-PCR. Pathological and serum CK-MB analysis to determine the extent of lesions and lesions. Results (1) Of the 12 ChKs tested, 9 were positive for VMC group, significantly more than 6 for normal myocardium, and 3 for ChKs (BLC.Eot and LARC) (2) ChKs expressed constitutively in MIP-2, MIG and IP-10 induced by CVB3 in 9 positive ChKs of VMC group expressed MIP-1β, MCP-1, MCP-2.Ltn four kinds of down-regulated expression of RANTES, compared with the normal control did not show significant differences for the FKN. (3) There was a certain difference in the expression and growth of ChKs. MIP-2 reached the peak at 4 d after infection, and then decreased. The expression of MCP-1 and RANTES increased at 9 d. FKN was stable at 9 d. (4) The expression of ChKs in the subacute early, middle, late and late myocardial tissues were significantly different. The ChKs expressed predominantly in the ChKs were IP-10, IP-10, MPC-1 and MCP-1, respectively. Conclusion ChKs in myocardium of VMC change in a clustering manner. The complexity of expression changes may be related to the complexity of pathogenesis. The predominant ChKs may play a more important role in the pathogenesis of viral myocarditis.