节点文献

Bc1-2和Bax基因产物在小鼠柯萨奇病毒性心肌炎心肌组织中的表达

Expression of Bcl-2 and Bax gene production in mice with coxsakievirus myocarditis

  • 推荐 CAJ下载
  • PDF下载
  • 不支持迅雷等下载工具,请取消加速工具后下载。

【作者】 韩波马沛然韩秀珍汪翼庄建新张建军

【Author】 HAN Bo, MA Peiran,HAN Xiuzhen,et al Shandong Provincial Hospital,Jinan 250021,P.R.China

【机构】 山东省立医院山东省立医院 250021济南250021济南

【摘要】 目的 探讨Bc1 2和Bax基因在病毒性心肌炎进展中的作用。方法 柯萨奇病毒B3 (CVB3 )感染12 5只雄性Balb/c小鼠 ,分别于d7、10、14、2 1、2 8随机取 2 0只实验组小鼠和 5只对照组小鼠处死 ,采用免疫组织化学方法检测CVB3 病毒性心肌炎小鼠不同时期心肌组织中Bcl 2和Bax蛋白表达情况。结果 病毒性心肌炎发病率为 86 % ,其中 80 %小鼠为轻、中度病变。正常对照组心肌中 ,无Bc1 2蛋白表达。在实验组中Bc1 2蛋白表达的动态变化与心肌病变积分呈显著正相关 (r =0 .93 P <0 .0 1) ,感染后 7~ 14d ,实验组小鼠心肌组织中Bax蛋白表达显著高于正常对照组 (P <0 .0 5 )。少数心肌浸润淋巴细胞表达Bc1 2和Bax。结论 Bc1 2和Bax基因参与病毒性心肌炎细胞凋亡的调控。

【Abstract】 Objective To investigate the role of Bcl 2 and Bax gene in the development of viral myocarditis(VM).Methods The total of 125 Balb/c mice were used in the experiment. Twenty mice in each experimental group (25 total in each group) were inoculated with 10 9 Tcid 50 CVB 3 0.12 ml and 5 mice (control) inoculated with saline. These mice were sacrificed on 7,10,14,21,28 days respectively after inoculated. Presence of apoptosis related proteins Bcl 2 and Bax in myocardium was determined by immunohistochemistry.Results The gross incidence of VM in the experiment group was 86 %.About 80 % of mice with VM showed mild to moderate histopathology. The dynamic changes of Bcl 2 expression level in experimental group showed significant positive correlation with the changes of myocardial histopathologic scores ( r=0.93 P <0.01).The amount of Bax protein increased prominently in the myocardium from experimental groups compared with control group( P <0.05). The infiltrating lymphocytes in the myocardium also expressed Bcl 2 and Bax.Conclusion Bcl 2 and Bax gene were involved in the regulation of apoptosis in VM

【关键词】 心肌炎病毒性小鼠细胞凋亡Bcl2Bax基因
【Key words】 virals myocarditismiceapoptosisBcl 2Baxgene
  • 【文献出处】 实用儿科临床杂志 ,Journal of Applied Clinical Pediatrics , 编辑部邮箱 ,2003年07期
  • 【分类号】R542.21
  • 【被引频次】11
  • 【下载频次】125
节点文献中: 

本文链接的文献网络图示:

本文的引文网络