人参总皂苷对体外培养肌管形态及Atrogin-1表达的影响

目的：慢性肾衰竭（CKD）尤其进入终末期透析的患者常并发以骨骼肌蛋白质-能量消耗为特征的营养不良,研究表明Atrogin-1激活是肌肉蛋白分解的关键步骤。本实验通过培养肌细胞,观察人参总皂苷的干预下,对糖皮质激素作用下肌细胞形态改变及Atrogin-1的表达的影响。方法：培养小鼠肌原细胞C2C12并使之融合成肌管,以不同浓度的地塞米松（0～10μm）和人参总皂苷（100μmol/L）刺激肌管后,镜下观察肌管形态改变,Westernblot检测Atrogin-1蛋白表达水平。结果：糖皮质激素地塞米松作用下,可剂量依赖性地使肌管变细,肌管Atrogin-1蛋白表达水平显著增高;在人参总皂苷干预后,肌管形态较地塞米松组增粗,同时肌管Atrogin-1蛋白降低（P〈0.05）。结论：人参总皂苷能够改善地塞米松作用下肌肉消耗,并下调肌管Atrogin-1蛋白表达水平。

Effects of Ginsenosides for the Cultured Myotube's Morphology and the Expression of Atrogin-1

Objective:Patients with chronic kidney disease(CKD) often complicated with malnutrition which characteristic skeletal muscle protein energy wasting.Early studies suggested that a key procedure was Atrogin-1 activation induced muscle proteins breakdown.In the present experiments,we observed the effects of ginsenosides for the myotube’s morphology and the Atrogin-1 expression treated with exogenous glucocorticoids(dexamethasone).Methods:Cultured mouse C2C12 myogenous cells and fused into myotubes,then treated with different concentrations of dexamethasone(0~10 μmol/L) and ginsenosides(100 μmol/L),observed myotube’s morphology by light microscopy,the protein expression of Atrogin-1 was measured by Western blot.Results:After treated with glucocorticoids,the myotube became thinner in a dose-dependent,and the expression of Atrogin-1 protein increased significantly(P<0.01).With the intervention of ginsenosides,the myotubes size was thicker compared with the dexamethasone groups,and the Atrogin-1 protein was decreased(P<0.01).Conclusion:The Ginsenosides can rescue the muscle wasting,and down-regulating Atrogin-1 protein expression induced by glucocorticoids.