摘要
目的:探讨Calpains在慢性阻塞性肺疾病(COPD)大鼠骨骼肌萎缩中的作用。方法:40只健康雄性Wistar大鼠随机分为COPD模型组及对照组,模型组采用气管内注入脂多糖加香烟烟雾染毒法建立大鼠COPD模型,HE染色法观察肺组织及骨骼肌(趾长伸肌、膈肌)组织的病理学改变;分别采用免疫组化和RT-PCR法测定骨骼肌组织中Calpains(μ-Calpain和m-Calpain)蛋白及mRNA的表达。结果:在COPD模型组大鼠观察到骨骼肌萎缩,对照组大鼠未见骨骼肌萎缩。与对照组比较,COPD模型组大鼠趾长伸肌及膈肌中μ-Calpain和m-Calpain蛋白及m-Calpain mRNA表达增强(P<0.05),而μ-Calpain mRNA的表达差异无统计学意义(P>0.05)。结论:Calpains在COPD模型大鼠骨骼肌中表达上调,可能参与COPD模型大鼠骨骼肌萎缩。
Aim： To study the role of Calpains in rat skeletal muscle atrophy of chronic obstructive pulmonary disease（ COPD）. Methods： Forty healthy male Wistar rats were randomly allocated into COPD group and control group. COPD model was established by dripping lipopolysacharide（ LPS） into trachea and exposing to cigarettes smoking. The pathological changes of lung tissue and skeletal muscle were observed by HE staining. Immunohistochemistry and RT-PCR were performed respectively to determine protein and mRNA expression of Calpain in skeletal muscle（ μ-Calpain and m-Calpain）.Results： Skeletal muscle atrophy was observed in COPD group instead of control group. Compared with control group,the expression of μ-Calpain and m-Calpain protein in extensor digitorum longus muscle and diaphragm of COPD group was enhanced（ P 0. 05）,as well as m-Calpain mRNA expression（ P 0. 05）. Conclusion： The expression of Calpains in skeletal muscle of rats COPD model upregulated. Calpains may be involved in COPD skeletal muscle atrophy.
出处
《郑州大学学报（医学版）》
CAS
北大核心
2016年第4期534-538,共5页
Journal of Zhengzhou University(Medical Sciences)
