摘要
目的 观察实验性病毒性心肌病小鼠心肌线粒体基因表达变化情况，探讨线粒体基因表达变化在病毒性心肌病中的发病作用。方法 用柯萨奇病毒B3m反复增量感染Balb／c小鼠，建立心肌病动物模型，用包容35852条基因的cDNA微矩阵芯片分析心脏组织特异的mRNA表达．筛选出明显差异表达的线粒体相关基因。采用原位末端脱氧核糖核苷酸转移酶介导的dUTP缺口末端标记法（TUNEL）观察心肌细胞凋亡情况。结果 共有31个心肌病小鼠心肌线粒体能量代谢相关基因、心肌细胞线粒体凋亡及相关调节基因明显差异表达。心肌病小鼠心肌细胞凋亡的数目明显高于对照组（t=8．85，P〈0．01）。结论 心肌线粒体功能受损伴有心肌细胞凋亡发生是病毒性心肌病的重要发病机制。
Objective To investigate the different mitochondrial gene expressions and the apoptosis in myocardium of experimental viral cardiomyopathy. Methods Balb/c mice were repeatedly infected with coxsackievirus B3m（CVB3m） to establish experimental model of dilated cardiomyopathy. Specific mRNA expression pattern in cardiomyopathy mouse heart was analyzed by cDNA microarray containing 35 852 genes. Apparently different expressions of mitochondria genes were selected. Terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling（TUNEL） were used to detect the changes of apoptosis. Results Expression of thirty one mitochondria genes were found to be associated with energy metabolism and apoptosis in cardiomyopathy mouse heart in comparison with normal control mouse cardiac tissues. The number of apeptotic myocardial cells in viral dilated cardiomyopathy group increased significantly in comparison with that in the normal control group （t = 8.85, P 〈 0.01 ）. Conclusions The abnormal functions of myocardium mitochondrium is associated with increased myocardial apoptosis, which is the key pathogenesis of viral cardiomyopathy.
出处
《中国地方病学杂志》
CAS
CSCD
北大核心
2007年第4期375-378,共4页
Chinese Jouranl of Endemiology
基金
黑龙江省科技厅攻关项目（GC02C133）：黑龙江省教育厅重点项目（115111211）
黑龙江省卫生厅课题（2005293）
关键词
心肌疾病
线粒体
心脏
基因表达
细胞凋亡
Myocardial diseases
Mitochondria, heart
Gene expression
Apoptosis
