MyoD家族蛋白在大鼠臂丛神经损伤后骨骼肌萎缩中的作用

The effect of MyoD family proteins on muscular atrophy induced by brachial plexus injury in rats

目的 探讨MyoD家族蛋白在去神经肌萎缩发生机制中的作用。方法 应用臂丛神经损伤后骨骼肌萎缩的大鼠模型 ,采用Western 印迹法检测MyoD ,肌细胞生成素蛋白表达的变化 ,通过逆转录聚合酶链式反应技术 (RT PCR)和Northern 印迹法研究MyoD和肌细胞生成素基因表达改变。结果 骨骼肌萎缩时 ,肌细胞生成素蛋白质的表达在去神经支配后 2 4h内先迅速上调 ,然后逐渐下降 ;而MyoD蛋白表达则在去神经支配后即开始逐渐下调。肌细胞生成素和MyoD基因在去神经支配后表达也明显下降。而氨哮素等药物可以分别上调肌细胞生成素和 /或MyoD的蛋白表达。结论 臂丛神经损伤后骨骼肌萎缩时肌细胞中MyoD家族蛋白质和肌细胞生成素表达的下调抑制了成肌细胞的分化融合修复作用 ,加剧了骨骼肌的萎缩。氨哮素等药物通过分别上调肌细胞生成素和

Objective To study the changes of MyoD/myogenin expression in atrophic muscle after injury of brachial plexus among rats and to explore the role of proteins of MyoD family in denervation induced muscular atrophy. Methods The brachial plexus was injured unilterally among 24 SD rats. Then the rats were randomly divided into four groups treated by perfusion into the stomach with FGb 761 (extract of ginkgo leaf), creatine, clenbuterol, or distilled water (control group) at the dosage of 100 mg -1 ·kg -1 ·d -1 for 8 weeks respectively. The changes of MyoD protein and myogenin were measured by Western blotting. The gene expression of MyoD and myogenin were determined by RT/PCR and Northern blotting. Results The expression of myogenin was upregulated within 24 hours after denervation then decreased in five days. On the seventh day, the expression of myogenin in the experimental side was weaker than in the control side. The expression of MyoD protein was downregulated soon after denervation. The expression of myogenin mRNA and MyoD was significantly downregulated after denervation. Clenbuterol, Egb, and creatine upregulated the expression of MyoD protein to a certain degree, creatine being the most effective and Egb being the least effective relatively. Clenbuterol and Egb upregulated the expression of myogenin in denervated muscle, clenbuterol being more effective. Creatine did not upregulate the expression of myogenin in denervated muscle remarkably. Conclusion After denervation, the expression of MyoD protein and myogenin decreases, which plays an important role in atrophy of denervated muscule. EGb, creatine and clenbuterol retard the denervation induced muscular atrophy by upregulating the expression of MyoD and/or myogenin.