运动训练和补肽抗大鼠骨骼肌衰老机制的初步研究

目的：观察6周负重训练和补充大豆多肽延缓I）_半乳糖大鼠骨骼肌衰老进程的作用效果，并探讨初步机制。方法：SD雄性大鼠3月龄60只，随机分为：6周安静组（C6）和6周模型组（M6）各6只，12周模型组（M12）、大负组（B12）、小负组（S12）、补肽组（P12）、补肽大负组（PB12）和补肽小负组（PS12）各8只，14月龄8只作为自然衰老组。分别于6周末和12周末处死大鼠，测试各项指标。结果：与C6相比，M6组大鼠各项指标出现不同程度的衰老表现；与M12组相比，负重或补肽可以显著提高各干预组大鼠骨骼肌超氧化物歧化酶（SOD）活力以及SOD/MDA，血清生长激素（GH）、胰岛素样生长因子I（IGF-I）含量和骨骼肌IGF-ImRNA表达量，降低骨骼肌丙二醛（MDA）含量，两种方式均具有明显的交互作用。结论：D-半乳糖6周皮下注射，能成功复制亚急性大鼠骨骼肌衰老模型，再经过6周负重训练或补肽均可以有效的缓解D-半乳糖大鼠骨骼肌的衰老进程，两者联合运用效果尤为明显。初步机制可能与减轻骨骼肌氧化应激以及脂质过氧化，纠正激素及相关因子的代谢紊乱，增加骨骼肌IGF-ImRNA的表达等有关。

The initial study on mechanism in postpone skeletal muscle aging process of D-galactose rats by movement training and soy polypeptide supplement

Objective： To observe the effect of the postpone in skeletal muscle aging process of D-galaetose rats by weight training and soy polypeptide supplement in 6 weeks, and disenss the initial mechanism. Method： Sixty male SD rats （three month old）were randomly as signed： 6 week control（ C6, ） and 6 week model（M6） 6 for each group, 12 week model（Mx2）, big load（B12）, small load（S12）, peptide（P12）, poptide ＋ big load（PB12） and peptide ＋ small load group（PSi2） 8 for each group, eight fourteen month rats were taken in the natural aging group. The rats were killed by the end of 6th week and 12th week, tested the indicators. Result： Compare with group C6, the indicators in group M6 showed aging in different levels; Compare with group M12, weight training or soy polypeptide supplement in all intervention groups e.ould increase the content of skeletal muscle superoxide dismutase（SOD）, SOD/MI）A, the serum growth hormone（GH）, insulin-like growth factor-1 （IGF-I）and skeletal muscle IGF-I mRNA, decreased the malondialdehyde （MDA） content of skeletal muscle, and they had notable in teraction. Conclusion： Rat skeletal muscle aging model can be copied successfully by D-galaetose hypodermic, and go on with 6-week weight training or soy polypeptide supplement, they can postpone the skeletal muscle aging process of D-galaetose rats, and the two interference way united can have more obvious effect. Its preliminary mechanism may be related to the reduction of skeletal muscle oxidative stress and lipid peroxidation, the correction of hormones and related factors metabolic disorders, the elevation of skeletal muscle IGF-I mRNA expression and