低频电刺激对坐骨神经损伤大鼠不同类型骨骼肌萎缩及内源性胰岛素样生长因子1表达的影响

背景：低频电刺激可以缓解骨骼肌的萎缩,但对肌纤维类型的影响尚不清楚,同时内源性胰岛素样生长因子1在萎缩后的肌纤维中的表达与电刺激的关系尚无公识。目的：观察低频电刺激对坐骨神经损伤大鼠不同类型骨骼肌纤维萎缩情况及内源性胰岛素样生长因子1表达的影响。方法：将健康雄性SD大鼠随机分为3组,切断模型组和电刺激组大鼠左侧坐骨神经制备失神经支配模型,适应5d后,对电刺激组大鼠损伤侧腓肠肌施以2Hz的电刺激,2次/d,每次持续20min,正常组和模型组常规饲养。30d后,取大鼠腓肠肌腹部,检测其肌纤维直径和数量;免疫组织化学法检测肌组织中胰岛素样生长因子1的水平。结果与结论：失神经支配后,大鼠腓肠肌Ⅰ、Ⅱ型肌纤维直径减小,Ⅰ型肌纤维数比例增大。与模型组比较,电刺激组大鼠腓肠肌Ⅰ、Ⅱ型肌纤维直径有所增大,尤以Ⅰ型肌纤维直径增大更明显（P〈0.05）。同时,电刺激组大鼠腓肠肌中胰岛素样生长因子1的表达也明显高于模型组（P〈0.05）。提示,2Hz的电刺激可促进胰岛素样生长因子1的表达,减轻Ⅰ型肌纤维的萎缩。

Effect of low frequency electric stimulus on skeletal muscle atrophy and endogenous insulin-like growth factor-1 expression after sciatic nerve transaction

BACKGROUND：Low frequency electric stimulus can release skeletal muscle atrophy,but the effect on muscle fiber type remains unclear.In addition,the relationship between electric stimulus and endogenous insulin-like growth factor-1（IGF-1） expression still not unified.OBJECTIVE：To investigate effect of low frequency electronic stimulus on different type skeletal muscle atrophy and endogenous insulin-like growth factor-1 after sciatic nerve transaction.METHODS：SD male rats were divided into 3 groups.Rats in the model and denervation groups were prepared for left sciatic denervation models,and stimulated by 2 Hz electrical stimulus,twice a day,20 minutes per time.Rats in the normal control and model groups were regularly raised.After 30 days,the animals were killed and the gastrocnemius was removed for detection of diameter and number of muscle fiber;expression of IGF-1 was measured by immunohistochemistry.RESULTS AND CONCLUSION：The diameter of type Ⅰ and Ⅱ fibers were decreased,and the type Ⅰ fiber proportion increased after denervation.Compared with the model group,the diameter of typeⅠand Ⅱ fibers were increased,especially more obviously in type Ⅰ fiber in the electronic stimulus group（P〈0.05）.Simultaneously,the IGF-1 expression of the electronic stimulus group was higher than that of the model group（P〈0.05）.The result demonstrated that 2 Hz electrical stimulus can up-regulate IGF-1 expression and alleviate the muscle atrophy of type Ⅰ fibers.