Zhaohui Wu1, Huiming Jin, Yudong Gu. 1. Department of Pathophysiology, Medical Center of Fudan University, Shanghai 200032, China.
Abstract
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 uniliterally 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 muscle. EGb, creatine and clenbuterol retard the denervation-induced muscular atrophy by upregulating the expression of MyoD and/or myogenin.
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 uniliterally 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 muscle. EGb, creatine and clenbuterol retard the denervation-induced muscular atrophy by upregulating the expression of MyoD and/or myogenin.