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MCP-1与CVB3相互作用参与病毒性心肌炎的发生 被引量:8

Interaction between monocyte chemoattractant protein-1(MCP-1) and CVB3 in pathogenesis of viral myocarditis
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摘要 目的 研究单核细胞趋化蛋白 - 1(MCP- 1)在 B3型柯萨奇病毒 (CVB3)诱导病毒性心肌炎 (VMC)发病中的作用。方法 构建小鼠 MCP- 1真核表达质粒 p VM。 CVB3腹腔注射雄性 BAL B/c小鼠 ,随机分四组 :单独 CVB3感染 VMC组 (A组 )、10 μg过表达 MCP- 1组 (B组 )、4 0 μg过表达 MCP- 1组 (C)和空质粒对照组 (D组 )。并设未感染生理盐水对照组 (E组 )和未感染过表达组 (F组 )。比较各组小鼠心脏重量和体重的比值 (HW/BW)、心肌组织病理学积分 (PS)、心肌组织病毒载量、血清 CK- MB水平。结果 与 E组相比 ,A组的 HW/BW、PS、血清 CK- MB和心肌组织病毒载量均有明显改变。表明 CVB3感染后小鼠出现一系列的体征改变。与 A组相比 B组的 HW/BW、PS、血清 CK- MB和心肌组织病毒载量均未呈明显改变。但 C组 CVB3载量明显降低 (P<0 .0 5 ) ,血清 CK- MB水平升高 (P<0 .0 1) ,而 HW虽然升高(P<0 .0 5 ) ,但是 HW/BW未呈明显的改变 (P>0 .0 5 ) ,PS升高 (P<0 .0 5 )。 D组与 A组相比 ,CVB3载量、血清 CK-MB水平、HW/BW和 PS均未呈明显的改变 (P>0 .0 5 )。 F组的 HW/BW和血清 CK- MB水平与 E组相比未呈现显著性差异 ,而 PS升高 ,但低于 A组 (P<0 .0 1)。结论 单独在心肌组织过表达 MCP- 1仅引起心肌组织学改变 。 Objective To investigate the role of monocyte chemoattractant protein 1(MCP 1) in viral myocarditis (VMC) induced by coxsackievirus Group B Type 3 (CVB3). Methods The plasmid pVM carrying murine MCP 1 coding gene was constructed. BALB/c mice inoculated intraperitoneally with CVB3 were divided into four groups including VMC group infected with CVB3 alone (group A), 10μg pVM over expression group (group B), 40μg pVM over expression group (group C) and blank plasmid (group D). And saline without CVB3 infection (group E) and over expression group without infection with CVB3 (group F) were used as controls. Ratio of mouse heart weight versus body weight (HW/BW), myocardial tissue pathological score of cardiac tissue (PS), the level of CK MB in serum and CVB3 loading of myocardial tissue were analyzed. Results There was much difference between group A and group E in HW/BW, PS, the level of CK MB in serum and CVB3 loading of myocardial tissue. In contrast there was no significant change between group A and group B in HW/BW, PS, the level of CK MB in serum and CVB3 loading of myocardial tissue. Whereas compared with group A, in group C CVB3 loading of myocardial tissue decreased obviously ( P <0.05), the level of CK MB in serum increased ( P <0.01), PS increased ( P <0.05), and there was not significant change in HW/BW ( P >0.05) though HW increased ( P <0.05). Compared with group A, CVB3 loading of myocardial tissue, the level of CK MB in serum, HW/BW and PS of group D all did not change much ( P >0.05). Compared with Group E, HW/BW and the level of CK MB in serum of group F did not show marked different ( P >0.05), whereas PS increased greatly but was lower than group A( P <0.05). Conclusions Over expression of MCP 1 alone in myocardium tissue without CVB3 infection could only lead to mild histological changes of myocardium but not cause the changes of HW/BW, the level of CK MB in serum and CVB3 loading of myocardial tissue. Over expression of MCP 1 in myocardium after CVB3 infection
出处 《中国心血管杂志》 2003年第5期305-309,共5页 Chinese Journal of Cardiovascular Medicine
基金 国家杰出青年科学基金 (3 992 5 0 3 1) 国家重点基础研究发展计划 (2 0 0 1CB5 10 0 0 6)资助项目
关键词 病毒性心肌炎 单核细胞趋化蛋白-1 发病机制 细胞浸润 viral myocarditis monocyte chemoattractant protein 1 pathogenesis cellular infiltration
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参考文献15

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