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病毒性心肌炎小鼠心肌与骨骼肌细胞线粒体损伤及其相关性(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2007年第1期
页码:
5-8
栏目:
基础研究
出版日期:
2007-01-01

文章信息/Info

Title:
Impairment and correlation of myocardial and skeletal mitochondria in mice with viral myocarditis
作者:
魏瑾1; 高登峰1; 牛小麟1; 刘健2; 陈明霞3
西安交通大学医学院：1. 第二附属医院心内科，陕西 西安 710004;2. 病理生理学教研室；3. 电镜室,陕西 西安 710061
Author(s):
WEI Jin1;  GAO Dengfeng1;  NIU Xiaolin1;  LIU Jian2;  CHEN Mingxia3
Department of Cardiology, Second Affiliated Hospital of Medical College, Xi′an Jiaotong University, Xi′an 710004, Shaanxi, China
关键词:
病毒性心肌炎; 柯萨奇病毒; 线粒体膜磷脂; 线粒体DNA
Keywords:
viral myocarditis; coxsackievirus B3; mice; mitochondrial membrane phospholipid; mitochondrial DNA
分类号:
R363
DOI:
-
文献标识码:
A
摘要:
目的 探讨病毒性心肌炎(VMC) 小鼠心肌与骨骼肌细胞线粒体损伤(线粒体膜磷脂脱失和线粒体DNA3867缺失)程度及二者的相关性。方法 50只BALB/c小鼠随机分为2组，实验组(40只) 腹腔注射内含柯萨奇B3病毒(Coxsackievirus B3，CVB3,TCID50＝108)的Eagle液制备VMC小鼠模型，另10只为对照组。分别于病毒感染后3、11和24 d行心肌和骨骼肌细胞线粒体膜磷脂脱失程度和mtDNA3867缺失率的测定，并用Spearman法对其进行相关分析。结果 实验组小鼠在病毒感染后3 d，可见心肌和骨骼肌细胞mtDNA3867缺失率显著高于对照组(P<0.05)，而线粒体膜磷脂脱失程度与对照组相比无显著性差异；病毒感染后11 d，心肌和骨骼肌细胞mtDNA3867缺失性损伤达高峰(P<0.05)，线粒体膜磷脂脱失程度亦显著高于对照组(P<0.05)；病毒感染后24 d，心肌和骨骼肌细胞线粒体膜磷脂脱失和mtDNA3867缺失程度与感染后11 d组比较无显著性差异，但与对照组和病毒感染后3 d组比较，仍有显著性差异 (P<0.05)。线粒体的上述损伤性改变在心肌和骨骼肌细胞呈一致性同步变化，且具有良好相关性(P<0.05)。结论 CVB3可显著损伤心肌和骨骼肌线粒体DNA和膜磷脂,两者损伤具有相关性，提示骨骼肌有望成为反映心肌细胞线粒体损伤的外周细胞“窗口”。
Abstract:
AIM To investigate the impairment of mitochondrial membrane phospholipid localization and DNA3867(mtDNA3867) deletion and its correlation between cardiac and skeletal muscle cells in mice with viral myocarditis. METHODS Fifty BALB/c mice were randomly divided into two groups: 40 in experimental group, with each injected 0.1 ml eagle liquids with Coxsackievirus B3(CVB3，TCID50＝108) intraperitoneally and 10 mice in control group with each given the same volume of eagle liquids. The loss of mitochondrial membrane phospholipid localization and mtDNA3867 deletion rate of cardiac and skeletal muscle cells were detected separately at the day 3, 11 and 24 after injection. The correlation of mitochondrial membrane phospholipid localization and mtDNA3867 deletion rate between the cells was analyzed using Spearman method. RESULTS At day 3 after injection, in both cardiac and skeletal muscle cells, mtDNA3867 deletion rate was significantly higher in experimental group as compared with that in the controls (P<0.05), but the localization of mitochondrial membrane phospholipid in the two groups showed no difference. At the day 11 after injection, mtDNA3867 deletion rate of the cardiac and skeletal muscle cells in experimental group increased to the peak level (P<0.05) and the loss of mitochondrial membrane phospholipid localization of the cells also increased markedly in experimental mice as compared with those in the controls (P<0.05). At the day 24 after injection, the damage of mitochondrial membrane phospholipid localization and mtDNA3867 deletion of the cells showed no differences as compared with the levels at the day 11 after injection, but still higher than that at the day 3 after injection (P<0.05). The lesions of mitochondrial membrane phospholipid localization and mtDNA3867 deletion were consistent and synchronistic between cardiac and skeletal muscle cells and were well correlated (P<0.05). CONCLUSION Mitochondrial DNA and mitochondrial membrane phospholipid of cardiac and skeletal muscle cells can be markedly damaged by CVB3. The skeletal muscle cells might act as peripheral “windows”, reflecting the mitochondrial damage levels of cardiac myocytes.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期：2006-04-06.通讯作者：魏瑾，副教授，主要从事心肌疾病基础与临床研究Email: weijin@mail.xjtu.edu.cn 作者简介：魏瑾
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