中文摘要：

目的探讨外源性心脏营养素-1（CT-1）延缓失神经骨骼肌萎缩的作用机制。方法将120只小鼠随机分为两组各60只，制作腓肠肌失神经模型后实验组腹腔注射CT-1 100μg／（kg·d），对照组注射等量CT-1溶媒，分别于给药后2、4、6周完整切取腓肠肌，检测骨骼肌细胞凋亡、蛋白代谢、兴奋一收缩耦联等相关指标。结果与对照组比较，观察组Fas mRNA表达降低、Bcl-2 mRNA表达增加、骨骼肌细胞凋亡率下降；肌细胞收缩蛋白中α-肌动蛋白、肌球蛋白重链Ⅱa mRNA表达增加；肌质网Ca^2＋-ATP酶水平升高；但泛素、RC2 mRNA表达水平及MeHis释放量无明显差异。结论外源性CT-1延缓失神经骨骼肌萎缩的机制为促进失神经骨骼肌结构性蛋白合成、抑制肌细胞凋亡、提高Ca^2＋-ATP酶水平等。

英文摘要：

Objective To investigate the action mechanism of cardlotrophln-1 （CT-1） on alleviating denervation atro- phy of skeletal muscle. Methods 120 mice were randomly divided into 2 groups, with 60 each, whose gastrocnemius muscle was denervated. The experimental group was injected CT-1 100 μg/（ kg · d） intraperitoneally , and the control group was injected with corresponding amount of vehicle. The gastrocnemius muscle was isolated respectively at 2, 4 and 6 weeks after denervation, and the relevant parameters such as myocyte apoptosis, protein metabolism and excitation-contraction couple in denervated skeletal muscle were assayed. Results Compared with the control group, the expressiom of Fas mRNA and apoptosis rate of myocogte in the experimental group decreased, the expression of Bcl-2 mRNA increased;the espression of α-action and MHC Ⅱ a mRNA and the content of Ca^2＋ -ATP increased. Conclusion CH can alleviate denervation atrophy of skeletal musde by inducing the synthesis of contractile protein, increasing the content of Ca^2＋ -ATPase and inhibiting myocyte apoptosis.