[Apoptosis in atrophic skeletal muscle induced by brachial plexus injury in rats]
- PMID: 11798813
[Apoptosis in atrophic skeletal muscle induced by brachial plexus injury in rats]
Abstract
Objective: To study the role of apoptosis and the expression of apoptosis-associated genes in skeletal muscle atrophy induced by brachial plexus injury in rats.
Methods: Rat models of skeletal muscle atrophy were established by cutting off brachial plexus of one upper limb. Apoptosis of muscular cells was investigated by TUNEL, flowcytometry, DNA electrophoresis and electromicroscopic observation. The apoptosis associated genes such as Fas, FADD, Caspase 8, c-myc, P53 and Bcl-2 were detected by immunohistochemical method (ABC) and Northern-blot.
Results: It was found with TUNEL and flowcytometry that the percentage of apoptotic muscle cell rose obviously in atrophic skeletal muscle (P < 0.05). DNA laddering could be seen in DNA gel electrophoresis of atrophic muscle after brachial injury. Morphologic changes of early stage in apoptotic cell could be seen under eletcromicroscope, such as the aggregation of chromosome, the expansion of nucleic cistern and the contraction of nucleus. Fas, FADD and Caspase genes were expressed highly and Bcl-2 gene was expressed lowly with immunohistochemical method in atrophic muscle. The results were all significantly different with that of the controls (P < 0.01). But the expression changes in P53 and c-myc genes were not obvious. The result of Northern-blot indicated that the mRNA of Fas gene rose and that of Bcl-2 gene decreased obviously (P < 0.01) in atrophic muscle induced by brachial plexus injury.
Conclusion: There are much more apoptotic cells in atrophic muscle induced by brachial plexus injury, and apoptosis plays an important role in its pathogenesis. The apoptotic signal maybe transmitted through Fas-->FADD-->Caspase 8, and the decrease in Bcl-2 gene expression aggravates the process.
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