慢性阻塞性肺疾病模型大鼠骨骼肌组织中 Caspase-12和 m-Calpain的表达

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。%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 .Skele-tal 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 immunohistochemi-cal 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 .