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目的:研究慢性阻塞性肺疾病(COPD)模型大鼠骨骼肌凋亡和JNK、ERK的表达,初步探讨JNK、ERK参与慢性阻塞性肺疾病骨骼肌细胞凋亡的机制。方法:将80只健康成年雄性Wistar大鼠分为COPD模型组及对照组,分别为60只和20只。用烟熏法建立COPD模型,对照组不熏香烟,再饲养至90d,称量大鼠的体重,将模型组的大鼠分为营养不良及营养正常两组,分组依据为小于对照组大鼠平均体重的90%为COPD营养不良大鼠。测定大鼠的一般情况、大鼠肺组织、气道的病理改变;趾长伸肌重量以及体重的变化;趾长伸肌病理变化;趾长伸肌的细胞凋亡率;JNK与ERK在组织切片上的表达;趾长伸肌的细胞凋亡率与JNK与ERK的相关性。结果:1模型组大鼠呈弓背状呼吸,饮食饮水减少,活动量显著减少,皮毛杂乱无光泽。而对照组大鼠各项指标均正常;2COPD组大鼠肺组织支气管管壁增厚,并且在肺组织周围有大量的炎性细胞浸润,肺泡壁变薄,肺泡腔扩大,符合COPD特征性的病理改变;3COPD模型组大鼠的趾长伸肌以及体重较对照组显著降低,且COPD营养不良组更明显(P<0.05);4COPD模型组大鼠趾长伸肌肌纤维明显萎缩;5COPD模型组大鼠骨骼肌细胞凋亡率明显高于对照组,且COPD营养不良组更明显(P<0.05);6COPD模型组大鼠JNK、ERK的表达率明显高于对照组,且COPD营养不良组更明显(P<0.05);7趾长伸肌的细胞凋亡率与JNK以及ERK的表达呈正相关(P<0.05)。结论:COPD模型组大鼠的体重下降以及骨骼肌萎缩可能与JNK和ERK介导的细胞凋亡有关。
AIM: To investigate the expression of JNK and ERK in skeletal muscle of rats with chronic obstructive pulmonary disease (COPD) and to explore the mechanism of JNK and ERK involved in the apoptosis of skeletal muscle cells in patients with chronic obstructive pulmonary disease. Methods: Eighty healthy adult male Wistar rats were divided into COPD model group and control group, 60 and 20 respectively. COPD model was established by smoking method, the control group did not smoke cigarettes, and then fed to 90 days, weighed the body weight of rats, the model group rats were divided into malnutrition and normal nutrition group, grouped according to less than the control group rats Ninety percent of the average body weight is COPD malnourished rats. The pathological changes of lung tissue and airway in rats were observed; the weight and body weight of extensor digitorum longus, the pathological changes of extensor digitorum longus, the apoptosis rate of extensor digitorum longus, the expressions of JNK and ERK in tissues The expression on the slice; the apoptosis rate of extensor digitorum longus and the correlation between JNK and ERK. Results: 1 The rats in the model group showed a bow-shaped breathing, reduced drinking water, significantly reduced the amount of activity, and disorderly and dull fur. While the control group rats were normal indicators; 2COPD group lung tissue bronchial wall thickening, and in the lung tissue around a large number of inflammatory cell infiltration, alveolar wall thinning, alveolar expansion, in line with the characteristics of COPD Pathological changes; 3COPD model rats long to long extensor and body weight was significantly lower than the control group, and COPD malnutrition group was more significant (P <0.05); 4COPD model rats long to narrow extensor muscle fibers significantly atrophy; 5COPD model group The apoptosis rate of skeletal muscle cells in rats was significantly higher than that in control group, and the malnutrition in COPD group was more obvious (P <0.05). The expression rates of JNK and ERK in 6COPD model group were significantly higher than those in control group, and more in COPD malnutrition group (P <0.05). There was a positive correlation between apoptosis rate and expression of JNK and ERK (P <0.05). Conclusion: The body weight loss and skeletal muscle atrophy in rats with COPD may be related to JNK and ERK-mediated apoptosis.