人参总皂苷对体外培养肌管形态及Atrogin-1表达的影响

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

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。

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 pro- teins 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 Ixmol/L） and ginsenosides （100 p^mol/L）, ob- served 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.