Impairment of Myocardial and Skeletal Mitochondria in Mice with Viral Myocarditis and Their Correlation

摘要

In order to investigate the impairment of mitochondrial membrane phospholipid localization and DNA~(3867) (mtDNA~(3867)) deletion and the correlation between cardiac and skeletal muscle cells in mice with viral myocarditis, 50 BALB/c mice were divided into two groups randomly. In experimental group (n=40), the mice were intraperitoneally injected with 0.1 mL Eagle liquid with CVB_3(TCID_(50)=10~8), while in the control group (n=10), the mice were subjected to equal volume of Eagle liquid. The impairment of mitochondrial membrane phospholipid localization and mtDNA~(3867) deletion rate of cardiac and skeletal muscle were detected separately at day 3, 11 and 24 after injection. The correlation of mitochondrial membrane phospholipid localization and mtDNA~(3867) deletion rate between cardiac and skeletal muscle cells cells was analyzed using Spearman method. At the day 3 after injection, in both cardiac and skeletal muscle cells, mtDNA~(3867) deletion rate was significantly higher in experimental group than in control group (P< 0.05), but the localization of mitochondrial membrane phospholipid showed no difference between two groups (P> 0.05). At day 11 after injection, the mtDNA~(3867) deletion rate of both cells in experimental group was increased to the peak level (P< 0.05), and the impairment of mitochondrial membrane phospholipid localization of both cells also increased markedly in experimental group as compared with control group (P> 0.05). At the day 24 after injection, the impairment of mitochondrial membrane phospholipid localization and mtDNA~(3867) deletion of both cells showed a recovery tendency, but still severer than those at the day 3 after injection (P< 0.05). The impairment of mitochondrial membrane phospholipid localization and mtDNA~(3867) deletion were consistent and synchronistic between cardiac and skeletal muscle cells, and showed good correlations (P< 0.05). The impairment of mitochondria plays an important role in the pathogenesis of viral myocarditis, and the skeletal muscle cells might act as a peripheral "window" to reflect the mitochondrial damage of cardiac myocytes.