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机构地区:[1]郑州大学第二附属医院呼吸内科,郑州450014
出 处:《郑州大学学报(医学版)》2014年第4期508-512,共5页Journal of Zhengzhou University(Medical Sciences)
摘 要:目的:探讨慢性阻塞性肺疾病(COPD)模型大鼠骨骼肌组织中Caspase-12和m-Calpain的表达情况。方法:将40只健康雄性Wistar大鼠随机分为COPD模型组和对照组各20只,模型组采用反复熏香烟加气道内滴猪胰弹性蛋白酶法建立COPD模型。采用TUNEL法测定2组大鼠骨骼肌(膈肌、趾长伸肌)细胞凋亡率,采用免疫组化法、RT-PCR检测2组大鼠骨骼肌内Caspase-12和m-Calpain蛋白及mRNA的表达。结果:与对照组相比,模型组大鼠膈肌、趾长伸肌的凋亡率增加(t=23.190和28.184,P<0.001),Caspase-12和m-Calpain蛋白和mRNA的表达亦增强(P<0.001)。模型组大鼠膈肌、趾长伸肌中Caspase-12和m-Calpain蛋白与mRNA的表达有关(r=0.885和0.787,P<0.05;r=0.862和0.774,P<0.05)。结论:Caspase-12可能参与COPD大鼠骨骼肌萎缩,m-Calpain可能通过激活Caspase-12参与该过程。Aim: To study the expression and significance of Caspase-12 and m-Calpain in COPD rats skeletal muscle atrophy. Methods: A total of 40 healthy male Wistar rats were randomly divided into model group( n = 20) and control group( n = 20). COPD model rats were copied by tabocco smoke inhalation and intracheally given PEE successfully. Skeletal muscle apoptosis rate was evaluated by TUNEL method. The expression of Caspase-12 and m-Calpain mRNA and protein in rat skeletal muscle were detected by reverse transcription-polymerase chain reaction( RT-PCR) and immunohistochemical respectively. Results: Compared with control group,the rates of muscle apoptosis in both diaphragmatic muscle and long extensor muscle digits of the model group were increased( t = 23. 190,28. 184; P 〈0. 001),and the expression of Caspase-12 and m-Calpain protein and mRNA were significantly enhanced( P 〈0. 001). Caspase-12 and m-Calpain had significant correlation( r = 0. 885,0. 787,P〈0.05; r = 0. 862,0. 774,P〈0.05). Conclusion: Reticulum apoptosis pathway,which involving Caspase-12 and m-Calpain,may be responsible for COPD rats skeletal muscle atrophy.
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