观察穴位电刺激预处理对长期超负荷训练后大鼠心肌细胞过度自噬的影响,进一步探讨穴位电刺激预处理保护运动心脏的作用机制.方法:根据超负荷概念建立超负荷训练动物模型,取15只雄性SD大鼠随机均分成对照组、超负荷训练组和穴位电刺激预处理组.对照组不予任何处理,超负荷训练组和穴位电刺激预处理组进行8周游泳训练.穴位电刺激预处理组每次训练前进行穴位电刺激,20min/次,取穴相当于内关和足三里.训练结束24h内取材,运用透射电镜观察大鼠心肌细胞自噬和凋亡情况.结果:超负荷训练组大鼠心肌细胞线粒体聚集、嵴断裂、空泡化,肌浆网扩张,核膜皱缩、核固缩、核仁消失,染色质聚集、边聚,凋亡小体、自噬体和自噬溶酶体大量生成；与超负荷训练组相比,穴位电刺激预处理组心肌线粒体聚集、嵴断裂、空泡化及核膜皱缩、染色质聚集、边聚等表现明显减轻,同时凋亡小体、自噬体和自噬溶酶体生成显著减少.结论:超负荷训练使大鼠心肌细胞出现过度凋亡和过度自噬,穴位电刺激预处理可以通过减轻心肌细胞凋亡程度、抑制其过度自噬实现保护心脏结构的目的.%Objective To probe the influence of preconditioning via electric acupoint stimulation on the autophagy of rat myocytes induced by overload training. Methods Fifteen male Sprague-Dauley rats were randomly and equally divided into three groups:group A(control group) .group B(overload training for 8 weeks alone),group C(preconditioning via electric acupoint stimulation on Neiguan(pc 6)and Zu-sanli(st 36)for 8 weeks before overload training). The autophagy and apoptosis of the myocytes were observed by the transmission electron microscopy within 24h after the last training. Results Overload training caused mitochondrial aggregation, cristae rupture, vacuolization, sarcoplasmic reticulum, nuclear membrane shrinkage,nuclear condensation,nucleoli disappearance,chromatin aggregation,margination, and a large number of apoptotic bodies and autophagosome. Preconditioning via electrical acupoint stimulation significantly relieved mitochondrial aggregation, ridge fracture, vacuolization, nuclear membrane shrinkage,chromatin aggregation,margination,and significantly reduce apoptotic bodies and autophagosome. Conclusion Overload training causes excessive apoptosis and autophagy of myocardial cells,whereas preconditioning via electrical acupoint stimulation can protect the heart by reducing the extent of myocardial cell apoptosis and inhibiting excessive autophagy.
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