葛根素治疗骨骼肌失神经萎缩机制与Cdk5相关性的实验研究  

A experimental study on the mechanism of puerarin in the treatment of denervated skeletal muscle atrophy and the correlation with Cdk5

作　　者：田峰[1] 季相禄[1] 王斌[1] 肖万安[1] 

机构地区：[1]中国医科大学附属盛京医院骨外科,辽宁沈阳110004

出　　处：《实用手外科杂志》2017年第1期91-94,共4页Journal of Practical Hand Surgery

基　　金：辽宁省教育厅科学研究项目（项目编号：12015589）

摘　　要：目的 探索葛根素在治疗大鼠周围神经损伤中的作用机制.方法 对28只体重在230~250 g的雄性大鼠制作失神经骨骼肌模型.实验动物随机分为四组.在葛根素治疗组中,对再灌注后-坐骨神经切断的大鼠给予50 mg/kg葛根素进行腹腔内注射,随后两天每24小时以同样的剂量注射.在抑制剂预处理组中,对大鼠制作失神经骨骼肌模型60 min之前给予30 mg/kg抑制剂进行静脉注射.失神经60 min后进行48 h的再灌注-注射,然后检测其细胞凋亡指数及Cdk5和p25的活性.结果 骨骼肌失神经,导致Cdk5和p25的活性升高、凋亡细胞数增多.葛根素可以降低细胞凋亡数及Cdk5和p25的活性.结论 失神经骨骼肌萎缩的缓解与Cdk5及p25受抑制相关,在失神经骨骼肌模型大鼠的治疗过程中,葛根素对Cdk5及p25的抑制作用是其神经保护性机制之一.Objective To explore the mechanism of Puerarin in the treatment of peripheral nerve injury in rats. Methods The model of denervated skeletal muscle was made in 28 rats（230~250 g）. The experimental animals were randomly divided into four groups. In the Puerarin treatment group, the rats were given intraperitoneal injection of 50 mg/kg puerarin after ciatic nerve transection, and the same dose was injected every 24 hours in the next two days. In Inhibitor pretreatment group, the rats were given the 30 mg/kg inhibitor by intravenous injection, 60 minutes before the denervated skeletal muscle model was made. After denervation for 60 minutes, reinjection for 48 hours, and then the apoptotic index and the activity of Cdk5 and p25 were detected. Results Denervation of skeletal muscle led to increased activity of Cdk5 and p25, and increased number of apoptotic cells. Puerarin can decrease the number of apoptotic cells and the activity of Cdk5 and p25. Conclusion The remission of denervated skeletal muscle atrophy is related to the inhibition of Cdk5 and p25. The inhibitory effect of Puerarin on Cdk5 and p25 is one of the neuroprotective mechanisms.

关 键 词：葛根素 失神经骨骼肌 CDK5 抑制剂 细胞周期蛋白B激酶抑制刺 

分 类 号：R685[医药卫生—骨科学]