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目的探讨吲哚美辛(IND)对慢性阻塞性肺疾病(COPD)大鼠模型骨骼肌细胞凋亡的影响。方法成年雄性Wistar大鼠100只,随机分为模型组80只,正常对照组20只。COPD大鼠模型造模成功后,模型组又分为COPD营养正常组(n=37)和COPD营养不良组(n=40),COPD营养不良组再随机分为A、B、C、D 4组,B、C、D组分别予以不同剂量IND灌胃[B组0.5 mg/(kg.d)、C组1.0 mg/(kg.d)、D组2.0 mg/(kg.d)]。A组、对照组和COPD营养正常组每天予以等量生理盐水灌胃。检测各组干预前后的体重,检测干预后膈肌和趾长伸肌的重量、细胞凋亡率和Bcl-2、Bax蛋白表达。结果 COPD营养不良各组的膈肌、趾长伸肌的细胞凋亡率和Bax蛋白表达明显高于COPD营养正常组和对照组(P<0.05),而膈肌、趾长伸肌的重量和Bcl-2蛋白表达明显低于COPD营养正常组和对照组(P<0.05)。IND干预后,B、C、D组大鼠体重增长速度均较A组增高,但只有C组的差异有统计学意义(P<0.05);C组膈肌、趾长伸肌的细胞凋亡率和Bax蛋白表达低于A、B、D组(P<0.05),Bcl-2蛋白表达高于A、B、D组(P<0.05)。结论细胞凋亡可能是COPD大鼠骨骼肌萎缩的重要原因,Bcl-2、Bax参与调节COPD大鼠模型的骨骼肌凋亡;吲哚美辛1.0 mg/(kg.d)干预可改善COPD营养不良大鼠模型骨骼肌细胞的凋亡。
Objective To investigate the effect of indomethacin (IND) on the apoptosis of skeletal muscle cells in a rat model of chronic obstructive pulmonary disease (COPD). Methods 100 adult male Wistar rats were randomly divided into model group (n = 80) and normal control group (n = 20). After the COPD model was successfully established, the model group was further divided into COPD normal nutrition group (n = 37) and COPD malnutrition group (n = 40). The COPD malnutrition group was randomly divided into A, B, C and D 4 Groups B, C and D were intragastrically given IND at different doses (group B 0.5 mg / (kg · d), group C 1.0 mg / (kg · d), group D 2.0 mg / (kg · d)]. Group A, control group and normal nutrition group of COPD were given the same amount of normal saline. The body weight of each group before and after intervention was measured. The weight of the diaphragmatic muscle and extensor digitorum longus, the apoptosis rate and the expressions of Bcl-2 and Bax protein were detected. Results The apoptotic rate and the expression of Bax protein in diaphragmatic muscle and extensor digitorum longum in COPD group were significantly higher than those in normal COPD nutrition group and control group (P <0.05). However, the weight of diaphragmatic muscle and extensor digitorum longus and Bcl- 2 protein expression was significantly lower than the normal nutrition group and control group COPD (P <0.05). After IND intervention, the body weight growth rate of rats in groups B, C and D was higher than that of group A, but there was only difference between group C and group C (P <0.05). The apoptosis rate of diaphragm and extensor digitorum longus in group C Bax and Bax were lower than those in A, B and D groups (P <0.05). The expression of Bcl-2 protein was higher than that in A, B and D groups (P <0.05). Conclusions Apoptosis may be the main reason of skeletal muscle atrophy in COPD rats. Bcl-2 and Bax are involved in the regulation of skeletal muscle apoptosis in COPD rats. Indomethacin 1.0 mg / (kg.d) can improve the nutrition of COPD rats Apoptosis in skeletal muscle cells of rat model.