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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 investigate the changes of Ca2 + concentration and MPTP opening rate in denervated skeletal muscle cells and the effect of nimodipine on them, and to find a new way to delay denervation skeletal muscle atrophy. Methods 72 Wistar rats were randomly divided into 3 groups: control group, model group and nimodipine group (abbreviated as treatment group). At 2, 14 and 28 days after operation, 8 rats in each group were sacrificed and the gastrocnemius muscles were sacrificed. The gastrocnemius wet mass ratio was measured. The changes of Ca2 + concentration were detected quantitatively by fluorescent indicator. The change of mitochondrial MPTP opening rate was observed by laser scanning confocal microscopy . Results The Ca2 + concentration and MPTP opening rate of the model group began to increase at 2 days after operation. With the prolongation of time (14d, 28d), Ca2 + concentration and MPTP opening rate continued to increase (P <0.05). The Ca2 + concentration and MPTP opening rate in the treatment group were lower than those in the same period (P <0.05), but they were always higher than those in the control group (P <0.05). There was a positive correlation between Ca2 + concentration and MPTP opening rate (r = 0.841, P <0.05). Conclusion Nimodipine can delay denervation skeletal muscle atrophy by inhibiting Ca2 + overload and MPTP opening.