【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—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Ca2+-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Ca2+-ATP酶水平等。更多还原

【Abstract】 Objective To investigate the action mechanism of cardiotrophin-1(CT-1) on alleviating denervation atrophy 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 Ⅱa mRNA and the content of Ca2+-ATP increased.Conclusion CH can alleviate denervation atrophy of skeletal musde by inducing the synthesis of contractile protein,increasing the content of Ca2+-ATPase and inhibiting myocyte apoptosis.更多还原