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目的:探讨凋亡在慢性低氧高二氧化碳小鼠骨骼肌萎缩中的作用及可能机制。方法:雄性C57BL/6小鼠16只,随机分成2组:低氧高二氧化碳4周(4HH)组和正常对照(NC)组(均n=8)。测量小鼠体重并观察体重变化;光镜观察小鼠骨骼肌细胞形态改变;透射电镜观察小鼠骨骼肌超微结构改变;用TUNEL法检测小鼠骨骼肌细胞凋亡。结果:4HH组小鼠体重增量明显低于NC组(P<0.05);光镜发现4HH组骨骼肌细胞局部萎缩,细胞间炎症细胞浸润增多;电镜发现4HH组骨骼肌细胞局部萎缩,线粒体肿胀、排列紊乱,线粒体膜部分破坏;与NC组相比,4HH组的凋亡指数明显升高(P<0.01)。结论:凋亡可能部分参与了慢性低氧高二氧化碳引起的小鼠骨骼肌萎缩。
Objective: To investigate the role of apoptosis in skeletal muscle atrophy in mice with chronic hypoxia and hypercapnia and its possible mechanism. Methods: Sixteen male C57BL / 6 mice were randomly divided into 2 groups: hypoxic hypercapnic 4h (4HH) group and normal control (NC) group (n = 8). The body weight of mice was observed and the changes of body weight were observed. Morphological changes of skeletal muscle cells were observed with light microscope. The ultrastructural changes of skeletal muscle were observed by transmission electron microscopy. The apoptosis of skeletal muscle cells was detected by TUNEL. Results: The body weight gain of 4HH group was significantly lower than that of NC group (P <0.05). The histopathology of 4HH group showed atrophy of skeletal muscle cells and increased infiltration of inflammatory cells in the 4HH group. Electron microscopy showed that 4HH group had atrophy of mitochondria, , Disordered, partially damaged mitochondrial membrane; compared with the NC group, 4HH group apoptosis index was significantly increased (P <0.01). Conclusion: Apoptosis may be partly involved in mouse skeletal muscle atrophy caused by chronic hypoxia and hypercapnia.