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复合蛋白锌对病毒致小鼠心肌损伤的保护作用
引用本文:王振先,郝芳之,徐成伟,李劲松,乔艳红,张兆华. 复合蛋白锌对病毒致小鼠心肌损伤的保护作用[J]. 山东大学学报(医学版), 2004, 42(1): 106-109
作者姓名:王振先  郝芳之  徐成伟  李劲松  乔艳红  张兆华
作者单位:山东大学第二医院儿内科,山东,济南,250000
摘    要:目的:探讨复合蛋白锌CPZ对病毒致小鼠心肌损伤的保护作用及其生化机制。方法:以柯萨奇病毒B3亲心肌变异株(CVB3m)诱导的BALBC心肌炎小鼠,观察CPZ对小鼠的发病情况、血清超氧化物歧化酶(SOD)活性及活性氧浓度;并利用光镜及电镜观察小鼠心脏的损伤情况。结果:服用CPZ组、CPZ合用VitC治疗组、VitC对照组、感染对照组小鼠感染CVB3m后病死率分别为10%、10%、50%、90%;服用CPZ组、CPZ合用VitC治疗组较感染对照组病死率明显降低(P<0.001),且稍低于VitC治疗组(P>0.05)。CPZ组及CPZ合用VitC治疗组病理改变(坏死灶数、炎性浸润灶数)均较感染对照组及VitC组明显减轻(P<0.001)。CPZ组及CPZ合用VitC治疗组血清SOD活性较感染组及VitC组明显增高,较正常组明显降低(P<0.001),活性氧浓度较感染组及VitC组明显降低,较正常组明显升高。结论:氧自由基在心肌炎发病中起重要作用,病毒性心肌炎早期应用CPZ,可通过提高SOD活性,清除自由基(又称活性氧)减轻心肌损害,降低感染动物的病死率,从而有效改善预后,且较VitC疗效好,为CPZ治疗病毒性心肌炎的临床应用提供了可能性。

关 键 词:小鼠  近交BALBC  心肌炎    锌化合物  超氧化物歧化酶  柯萨奇病毒B型  
文章编号:1671-7554(2004)01-0106-04
修稿时间:2002-02-05

Study on the protective effect and mechanism of compound protein zinc (CPZ) on mice cardiac muscle damage virus-induced in mice CV B3m myocarditis
WANG Zhen-xian,HAO Fang-zhi,XU Cheng-wei,et al. Study on the protective effect and mechanism of compound protein zinc (CPZ) on mice cardiac muscle damage virus-induced in mice CV B3m myocarditis[J]. Journal of Shandong University:Health Sciences, 2004, 42(1): 106-109
Authors:WANG Zhen-xian  HAO Fang-zhi  XU Cheng-wei  et al
Abstract:Objective: To investigate the protective effect and mechanism of compound protein zinc (CPZ) on mice cardiac muscle damage caused by virus. Methods: Superxide dismetase (SOD) activities and oxygen free radical levels of acute myocarditis mice revulsive CVB3 were assayed, and damages of mouse heart under light and electric microscopes. Results: Fatality rates of CPZ, CPZ plus VitC, VitC and the infected control group are 10%,10%,50% and 90%, respectively; tatality rates of CPZ, CPZ plus VitC groups decreased sighificaufly than those of the infected control group, the fatality rates of CPZ and CPZ bles VitC group were basicly the same as VitC group (P>0.05). Pathological changes(amount of myocardial cellular infiltration and myocardial necrosis)of all treated groups with CPZ sigmficaufly lightened than those of the infected control and VitC group (P<0.001). SOD activities of all CPZ treated groups inereased signifucanfly than those of the infected control and VitC group, but decreased than normal group (P<0.001),the oxygen free radical levels decreased significautly than those of the infected control group and VitC group but elevated than normal group (P<0.001). Conclusion: Oxygen free radical play an important role in virus myocarditis. Application of CPZ in the early viral myocarditis, could obviously decrease cardiac muscle damages and fatality rate of infection mice by increasing SOD activities and cleaning out oxygen free radical, accordingly , efficiently improve prognosis, and advantage than VitC,offers possibility for treating virus myocarditis with CPZ.
Keywords:Mice   inbreed BALB C  Myocarditis   mice  Zinc compounds  Superoxide dismutase  Enterovirus B   mice
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