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补阳还五汤对大鼠失神经肌萎缩的影响与机制研究 被引量:8

Effect of Buyang Huanwu Decoction on the Denervated Muscle Atrophy of Rats and Investigation for Mechanism
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摘要 目的研究补阳还五汤(BYHWD)对大鼠胫前肌失神经肌萎缩的影响,并探讨其机制。方法建立大鼠腓总神经损伤模型,术后大鼠随机分为假手术组,模型组,补阳还五汤高、中、低剂量组,甲钴胺组,共6组每组10只。术后每日灌胃,给药18 d后,石蜡包埋切片,形态学分析,计算胫前肌湿重比,并用实时荧光定量聚合酶链反应检测Angptl4与PI3K基因的表达。结果①湿重比:与模型组相比,补阳还五汤高、中剂量组显著增高(P<0.05或P<0.01)。②运动终板:假手术组为棕黑色,形状为椭圆形或圆形,着色均匀,补阳还五汤高剂量组与甲钴胺组边缘较粗糙;补阳还五汤中、低剂量组与模型组数量逐渐减少,且形态不规则,边缘不光滑;着色也逐渐变浅。③Angptl4与PI3K mRNA;补阳还五汤高、中剂量组与模型组相比均有统计学差异(P<0.01或P<0.05)。结论补阳还五汤能明显延缓胫前肌湿重比降低与运动终板的退变,从而有效防止失神经肌萎缩的发生,其机制可能是通过增加Angptl4、PI3K基因表达而实现的。 OBJECTIVE To explore the influence of buyang huanwu decoction(BYHWD) on the denervated tibial muscle atrophy of rats and to study the mechanisms of BYHWD defering denervated muscle atrophy of rats. METHODS Sprague-Dawley rats were subjected to common peroneal nerve crush model, then they were randomly divided into sham operation group, model group, BYHWD high-dose, medium-dose, low-dose groups, mecobalamin group (positive control). Each group has ten rats. The gavage lasted for 18 d. After that, performed slice, staining and analysis morphology were performed. The wet weight ratio of tibial muscle was measured. At the same time, qRT-PCR and western-blot detect the differential expression of Angptl4 and PI3K in the high-dose group of BYHWD and model group. RESULTS ①Wet weight ratio: BYHWD high and medium-group increased significantly compared with model group (P 〈 0. 01 or P 〈 0. 05 ). ② The motor end-plate :the sham operation group is sepia, oval or round; the BYHWD high-dose group and mecobalamin group has little chage; the BYHWD medium-dose group, low-dose group and the model group has lessen, shape is not rule gradually, the edge is rough, coloring is slight gradually. ③the expression of Angptl4 and PI3K: compared with model group, the BYHWD high and medium-group increased significantly( P 〈 0. 05 or P 〈 0. 01 ). CONCLUSION BYHWD can effectively delay denervated tibial muscle atrophy of rats by increasing the wet weight ratio and defering the degeneration of the motor end-plate which mechanism maybe increase Angptl4 and PI3K expression.
出处 《中国药学杂志》 CAS CSCD 北大核心 2014年第9期726-730,共5页 Chinese Pharmaceutical Journal
基金 国家自然科学基金青年基金资助项目(81302890) 高等学校博士学科点专项科研基金面上项目(20123237120004) 江苏省自然科学基金面上项目(BK2011816) 江苏省高校自然科学基金面上项目(13KJB360003) 南京中医药大学青年自然基金(12XZR09)
关键词 补阳还五汤 失神经 肌萎缩 大鼠 胫前肌 Angptl4 PI3K buyang huanwu decoction denervation muscle atrophy rat tibial muscle Angpt14 P13 K
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