首页> 中文期刊> 《中国康复理论与实践》 >电针对失神经骨骼肌萎缩大鼠胰岛素样生长因子1、肌肉生长抑制素及肌卫星细胞增殖的影响

电针对失神经骨骼肌萎缩大鼠胰岛素样生长因子1、肌肉生长抑制素及肌卫星细胞增殖的影响

         

摘要

目的:探讨电针延缓失神经骨骼肌萎缩的可能机制。方法49只雄性Sprague-Dawley大鼠随机分为正常组(A组, n=7)、自然恢复组(B组, n=21)和电针治疗组(C组, n=21)。A组不做处理,其余两组切断坐骨神经制备失神经性骨骼肌萎缩模型。术后1 d,C组术侧腓肠肌给予电针足三里、承山治疗每天1次。术后7 d、14 d、21 d分别测定术侧腓肠肌湿重比,HE染色测定肌纤维直径及截面积,Western blotting检测胰岛素样生长因子1(IGF-1)、肌肉生长抑制素(Myostatin)以及增殖细胞核抗原(PCNA)蛋白,RT-PCR检测IGF-1、Myostatin和PCNA基因表达。结果与A组比较,B组和C组腓肠肌湿重比、肌纤维截面积及直径均显著下降(P<0.001),但C组显著高于B组(P<0.001)。C组IGF-1、PCNA蛋白和基因表达高于B组(P<0.05),Myostatin蛋白和基因表达低于C组(P<0.05)。结论电针能有效促进IGF-1的表达,抑制Myostatin的表达,从而促进肌卫星细胞增殖。这可能是电针延缓失神经性骨骼肌肌萎缩的机制之一。%Objective To observe effects and mechanism of electroacupuncture (EA) on denervated skeletal muscle atrophy. Methods Forty-nine male Sprague-Dawley rats were randomly divided into normal group (group A, n=7), natural recovery group (group B, n=21) and EA group (group C, n=21). The groups B and C, established the model of denervated skeletal muscle atrophy by transecting the sciatic nerve of rats, were divided into subgroups of 7 days, 14 days, 21 days postoperation, seven in each subgroup. Electroacupuncture was given to the group C at Zusanli (ST36) and Chengshan (BL57) once a day since 24 hours after modeling. The muscle wet weight ratio of the affected gas-trocnemius was determined. Cross-sectional area and fiber diameter of the gastrocnemius were measured with HE staining. The expression of insulin-like growth factor-1 (IGF-1), Myostatin and proliferating cell nuclear antigen (PCNA) protein and gene in the gastrocnemius were detected with Western blotting and RT-PCR. Results The wet weight ratio, cross-sectional area and fiber diameter were less in the groups B and C than in the group A (P<0.001), and they were more in the group C than in the group B (P<0.001). Compared with the group B, the pro-tein and gene of IGF-1, PCNA increased in the group C (P<0.05), while the Myostatin decreased (P<0.05). Conclusion Electroacupuncture can increase the expression of IGF-1 and decrease the expression of Myostatin, to promote the proliferation of satellite cell, which may re-late with the prevention of denervated skeletal muscle atrophy.

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