Bcl-2及Bax表达与COPD大鼠骨骼肌细胞凋亡的相关性
投稿时间:2010-11-29  修订日期:2010-12-14  点此下载全文
引用本文:周兰英,孙圣华,李定梅,杨勇,唐文祥,郑莉茗,曾祥伯.Bcl-2及Bax表达与COPD大鼠骨骼肌细胞凋亡的相关性[J].医学研究杂志,2011,40(8):104-108
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作者单位
周兰英 湖南省怀化医学高等专科学校 
孙圣华 中南大学湘雅三医院呼吸科 
李定梅 湖南省怀化医学高等专科学校 
杨勇 湖南省怀化医学高等专科学校 
唐文祥 中南大学湘雅三医院呼吸科 
郑莉茗 湖南省怀化医学高等专科学校 
曾祥伯 湖南省第二人民医院 
基金项目:湖南省怀化医学高等专科学校资助项目(2010KY07)
中文摘要:目的探讨慢性阻塞性肺疾病(COPD)模型大鼠骨骼肌Bcl-2 、Bax表达与骨骼肌细胞凋亡的关系。方法100只健康Wistar大鼠随机分为模型组80只,正常对照组(NC)20只。模型组采用熏香烟和气管内滴注猪胰蛋白酶(PEE)法建立COPD模型大鼠,以低于NC大鼠平均体重的90%作为判断发生营养不良的标准,将COPD模型大鼠分为COPD营养不良组(NM)和COPD营养正常组(MC)。取大鼠骨骼肌(膈肌、趾长伸肌)制备石蜡切片,分别采用TUNEL法测定骨骼肌细胞凋亡率,免疫组织化学法测定骨骼肌Bcl-2、Bax表达,Image-Pro Plus version 6.0图像系统测定Bcl-2、Bax蛋白表达强度。结果NM大鼠膈肌、趾长伸肌的凋亡率高于NC和MC(P<0.05);NM大鼠膈肌、趾长伸肌Bcl-2的表达均低于NC和MC(P<0.05);NM膈肌、趾长伸肌的Bax表达均强于MC和NC(P<0.05)。结论COPD模型大鼠可能存在骨骼肌细胞凋亡,Bcl-2、Bax可能参与COPD模型大鼠骨骼肌细胞凋亡。
中文关键词:慢性阻塞性肺疾病  骨骼肌  细胞凋亡  Bcl-2  Bax
 
Study on Relationship between Expressions of Bcl-2 and Bax and Skeletal Muscle Apoptosis in COPD Rats
Abstract:ObjectiveTo study the relationship between expressions of Bcl-2 and Bax and skeletal muscle apoptosis in COPD rats.Methods100 healthy male adult Wistar rats were randomly divided into two groups including model group (n=80) and normal control group (NC,n=20).COPD model rats were copied by tabocco smoke inhalation and intracheally given PEE successfully.COPD model rats were redivided into two groups including malnutrition COPD group(MC)which was lower than 90% of the mean body weight of NC and non-malnutrition COPD group(NM).With keletal muscle(diaphragmatic muscle and long extensor muscle digits)from all tested rats as experimental materials,the rates of muscle apoptosis,expression of related protein of Bcl-2 and Bax were measured by TUNEL method,immunohistochemical method and Image-Pro Plus version 6.0 systerm respectively.ResultsThe rates of muscle apoptosis in both diaphragmatic muscle and long extensor muscle digits of the MC were higher than those of NM and NC(P<0.05).The expression of Bcl-2 in MC was lower than that of NM and NC(P<0.05).The expression of Bax in MC were significantly higher than that of NM and the NC(P<0.05).ConclusionApoptosis is the important mechanism of skeletal muscle atrophy in COPD model rats probably.The genes Bcl-2 and Bax are the factors to adjust the muscle apoptosis in COPD model rats.
keywords:Chronic obstructive pulmonary disease  Skeletal muscle  Apoptosis  B cell cymphoma /leukemia-2  Bcl-2 associated x protein
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