杜仲总黄酮对大鼠神经源性肌萎缩的影响

Effect of total flavones of cortex eucommia on neurogenic muscular atrophy rat

目的观察杜仲总黄酮对大鼠神经源性肌萎缩的治疗效果。方法以30只1月龄雌性SD大鼠作为实验动物,随机选取24只大鼠夹伤右后肢坐骨神经制作神经源性肌萎缩模型,并分为4组:模型组、杜仲总黄酮低、中、高剂量组;不做坐骨神经夹伤处理的剩余6只大鼠作为对照组。在自由饮食状态下,模型组和对照组不予以灌胃处理,杜仲总黄酮低、中、高剂量组采用灌胃方式分别喂饲TFE 50、100、200 mg/kg/d,共4周。实验处理结束后,各组大鼠麻醉处死取右后肢腓肠肌称重并制作HE染色切片测量肌细胞横截面积,Western blot方法检测肌肉组织中肌肉抑制素(MSTN)蛋白和凋亡相关蛋白Bcl-2、Bax的表达。结果与对照组相比膜型组的腓肠肌重量和肌细胞的横截面积明显减少;给予杜仲总黄酮的各组中腓肠肌重量和肌细胞的横截面积也減少,但其减少程度较模型组降低,且与剂量呈正相关。与对照组相比,模型组中MSTN蛋白的表达量明显增多;杜仲总黄酮各组中MSTN蛋白与对照组相近,且各组间的表达量无统计学差异。与对照组相比,模型组中促凋亡蛋白Bax表达量明显增加,而抑凋亡蛋白Bcl-2表达量明显下降;杜仲总黄酮的各组中,当给予剂量达到100 mg/kg/d及以上时可明显抑制Bax的表达量和促进Bcl-2的表达量(P<0.05)。结论杜仲总黄酮能改善神经损伤后SD大鼠的肌萎缩症状,可以通过调节MSTN蛋白、凋亡相关蛋白Bax和Bcl-2的表达量而减少其肌肉重量和肌细胞大小的损失。

Objective To observe the effect of total flavones of Cortex Eucommia（TFE） on neurogenic muscular atrophy rats.Methods 30 one-month old female Sprague Dawley rats were used.24 rats were picked randomly to crush right sciatic nerves and divided into model group（MOD）,group of low dose of TFE（TFEL） group of medial dose of TFE（TFEM） and group of high dose of TFE（TFEH）.The rest rats without crush sciatic nerves were used as control group（CON）.The rats of MOD and CON groups were fed food and water freely without extra administration.The rats of TFEL TFEM and TFEH groups（TFE groups） were given TFE at 50,100 and 200mg/kg/d,respectively via intragastric administration for 4 weeks.All rats were sacrificed after anaesthesia.Gastrocnemius muscles of right hind leg of rats was cut to measure the weight and size of muscle cells.In addition,Myostatin（MSTN） protein and apoptosis related protein Bax and Bcl-2 were examined by Western blot.Results Compared with control group,the muscle mass and cells＇ size of model group were declined markedly.When TFE groups were administrated TFE,alleviative effects emerged and had a positive correlation with the concentration of TFE.Compared with control group,the expression of MSTN of model group was higher.The expressions of MSTN of three TFE groups were similar to control group and each TFE group had no difference.The expression of Bax of model group was higher while Bcl-2 was lower than control group.When the doses of TFE were greater than 100 mg/kg/d,the expression of Bax was lower and Bcl-2 was higher than those in model group（P〈 0.05）.Conclusion TFE alleviates the muscular atrophy symptom of SD rats after their sciatic nerve crush possibly mediated through regulating the expression of MSTN,Bax and Bcl-2 and ultimately resulting in less loss of muscle mass and cells＇ size.