摘要
通过给ＢＡＬＢ／Ｃ小鼠腹腔接种ＣＶＢ３ｍ后３、６、９、１２、１５、３０天分批随机处死小鼠，取心脏进行检测发现：感染后９～１５天，病毒性心肌炎（ＶＭＣ）检出率可达９２．３０％。感染后３～９天，心肌中可分离出病毒，而病毒核酸（ＣＶＢＲＮＡ）可持续存在于感染后３个月。应用电镜、原位末端标记法（ＴＵＮＥＬ）及免疫组化法检测发现：ＶＭＣ鼠心肌中可见心肌细胞和血管内皮细胞凋亡及ＴＧＦ－β１和Ｃ－ｍｙｃ蛋白的表达。感染后９～１５天，三者阳性率分别为７５．８６％、７２．４１％和８２．７６％，且分布区域基本一致。Ｐ５３蛋白摄影性率为１．９２％，无统计学意义。实验结果表明：ＣＶＢ３ｍ可诱发ＢＡＬＢ／Ｃ小鼠ＶＭＣ，而细胞凋亡可能参与ＶＭＣ的发生与发展。ＣＶＢ３ｍ、ＣＶＢＲＮＡ、ＴＧＦ－β１和Ｃ－ｍｙｃ蛋白可能在ＶＭＣ细胞凋亡调控机制中起一定作用。进而揭示细胞凋亡可能与ＤＣＭ。
The CVB 3m was inoculated into abdominal cavity of BALB/C mice in this experiment,then the mice were killed in 3,6,9,12,15,30 days separately.The rate of viral myocarditis (VMC) was 92.30% after 9～15 days of virus infection.After 6～9days of CVB 3m infection,vital virus was separated form myocardium.But CVB RNA presented continually after 3 months in myocardium.The apoptosis and expression of C myc and TGF β 1 were found in the cells of myocardium of infected mice by electronic microscope,TUNEL and immunohistochemical method.The results of experiment indicated that VMC of BALB/C mice can be induced by CVB 3m .Apoptosis may participate in occurrence and development of VMC.CVB 3m ,CVB RNA,C myc and TGF β 1 may participate in adjustment of apoptosis of VMC.
出处
《中国地方病学杂志》
CAS
CSCD
1997年第4期203-206,共4页
Chinese Jouranl of Endemiology
关键词
细胞凋亡
病毒性心肌炎
Apoptosis\ Virus\ Myocarditis\ Gene
