尼莫地平对大鼠失神经骨骼肌细胞萎缩的延缓作用  

The effect of Nimodipine on denervated skeletal muscle atrophy in rats

作　　者：贾奇[1] 梁炳生[1] 杨森[1] 何祥乐[1] 

机构地区：[1]山西医科大学第二医院骨科,太原030001

出　　处：《中国医疗前沿》2011年第4期40-41,70,共3页China Healthcare Innovation

摘　　要：目的探讨失神经骨骼肌细胞中Ca2+浓度和MPTP开放率的变化及尼莫地平对它们的影响,寻找延缓失神经骨骼肌萎缩的新途径。方法采用右下肢失神经腓肠肌动物模型,将72只Wista大鼠随机分为3组:对照组,模型组、尼莫地平组(简称治疗组)。在术后2、14、28d每组取8只大鼠处死取双侧腓肠肌,测腓肠肌湿质量比,用荧光指针定量检测Ca2+浓度的变化,激光共聚焦显微镜观察标本细胞线粒体MPTP开放率的变化。结果模型组术后2d Ca2+浓度和MPTP开放率已经开始增加,随着时间延长(14d、28d),Ca2+浓度和MPTP开放率均持续增加(P<0.05)。治疗组术后Ca2+浓度和MPTP开放率均低于同期模型组(P<0.05),但却始终高于同期对照组的表达水平(P<0.05)。Ca2+浓度与MPTP开放率呈正相关(r=0.841,P<0.05)。结论尼莫地平可以通过抑制Ca2+超载和MPTP的开放来延缓失神经骨骼肌萎缩。Objective To explore concentration of calciumion and mitochondrial permeability transition pore in denervated skeletal muscle in rats and the intervention effects with Nimodipine.Methods Wista rats with denervation were served as experiment models.Seventy-two Wistar rats were randomly divided into the normal control group,denervated group and Nimodipine treatment group after denervation.After 2,14 and 28 days,we evaluated the concentration of calciumion of the three groups by fluorescence probe,and detected the mitochondrial permeability transition pore by laser microscope.Results Concentration of calciumion and mitochondrial permeability transition pore in denervated skeletal muscle were up-regulated at 2,14 and 28 days after denervation（P0.05）.Moreover,the concentration of calciumion and mitochondrial permeability transition pore in Nimodipine group remarkably reduced compared with denervated group（P0.05） at each time point,but still more than that of the normal control group（P0.05）.The positive correlation among Concentration of calciumion and open mitochondrial permeability transition pore（r=0.841,P0.05）.Conclusion Nimodipine may help prevent denervated skeletal muscle atrophy through calciumion /MPTP pathway.

关 键 词：失神经 肌萎缩 尼莫地平 Ca2+超载 MPTP 

分 类 号：R322.74[医药卫生—人体解剖和组织胚胎学] R685.5[医药卫生—基础医学]