凋亡在慢性低氧高二氧化碳小鼠骨骼肌萎缩中的作用

Apoptosis on Skeletal Muscle Atrophy of Mice Induced by Chronic Hypoxic Hypercapnia

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。

Aim： To explore apoptosis on the skeletal muscle atrophy of mice induced by chronic hypoxic hypercapnia. Methods： 16 male C57BL/6 mice were randomly divided into two groups： hypoxic hypercapnia 4-week （4HH） group and normal control （NC） group. The body weight of the mice was measured. The morphological changes were observed in the skeletal muscle of the mice by light microscope. The ultramicrostructures of mouse skeletal muscle were observed by transmission electron microscope. The apoptosis in mouse skeletal muscle was detected with TUNEL staining. Results： The elevation of body weight （WA） of mice in 4HH group was lower than that in NC group （P〈0.05）. There were skeletal muscle atrophy and inflammatory cells under light microscope. The mitochondrial ultramicrostructures of the skeletal muscle were abnormal by transmission electron microscope. Compared with NC group, apoptosis index （AI） increased significantly （P〈0.01） in 4HH group. Conclusion： Apoptosis may contribute partly to skeletal muscle atrophy of mice induced by chronic hypoxic hypercapnia.