中国医药
中國醫藥
중국의약
CHINA MEDICINE
2012年
7期
821-823
,共3页
王慧%罗勇%韩锋锋%张悦%杨天云%徐卫国
王慧%囉勇%韓鋒鋒%張悅%楊天雲%徐衛國
왕혜%라용%한봉봉%장열%양천운%서위국
肺疾病,慢性阻塞性%肿瘤坏死因子α%骨骼肌%泛素蛋白酶体途径
肺疾病,慢性阻塞性%腫瘤壞死因子α%骨骼肌%汎素蛋白酶體途徑
폐질병,만성조새성%종류배사인자α%골격기%범소단백매체도경
Pulmonary disease,chronic obstructive%Tumor necrosis faclor-α%Skeletal muscle%Ubiquitin-dependent proteolytic pathway
目的 研究慢性阻塞性肺疾病(COPD)模型大鼠骨骼肌组织泛素蛋白连接酶Atrogin-1的表达,以及肿瘤坏死因子α(TNF-α)对其的影响,探讨COPD大鼠骨骼肌萎缩的机制.方法 30只SD大鼠按随机数字表法分为对照组(A组)、COPD组(B组)和COPD+ TNF-α组(C组),每组10只,单纯烟熏法制成COPD大鼠动物模型,分离趾长伸肌,B组和C组分别给予不含和含TNF-α( 10 μg/L)的孵育液进行离体有氧孵育.实时定量聚合酶链反应(PCR)和蛋白质印迹检测Atrogin-1 mRNA和蛋白的表达.结果 B组和C组Atrogin-1的mRNA表达分别为A组的(1.48 ±0.27)倍和(2.05 ±0.44)倍(均P＜0.01),同时C组明显高于B组(1.41±0.32倍,P＜0.05).B组和C组Atrogin-1蛋白表达也明显高于A组(0.80±0.09和0.96±0.16比0.63 ±0.14,均P＜0.01),B组和C组蛋白表达差异也有统计学意义(P＜0.05).结论 COPD模型大鼠骨骼肌组织Atrogin-1表达增强,且TNF-α可使Atrogin-1表达上调.
目的 研究慢性阻塞性肺疾病(COPD)模型大鼠骨骼肌組織汎素蛋白連接酶Atrogin-1的錶達,以及腫瘤壞死因子α(TNF-α)對其的影響,探討COPD大鼠骨骼肌萎縮的機製.方法 30隻SD大鼠按隨機數字錶法分為對照組(A組)、COPD組(B組)和COPD+ TNF-α組(C組),每組10隻,單純煙熏法製成COPD大鼠動物模型,分離趾長伸肌,B組和C組分彆給予不含和含TNF-α( 10 μg/L)的孵育液進行離體有氧孵育.實時定量聚閤酶鏈反應(PCR)和蛋白質印跡檢測Atrogin-1 mRNA和蛋白的錶達.結果 B組和C組Atrogin-1的mRNA錶達分彆為A組的(1.48 ±0.27)倍和(2.05 ±0.44)倍(均P＜0.01),同時C組明顯高于B組(1.41±0.32倍,P＜0.05).B組和C組Atrogin-1蛋白錶達也明顯高于A組(0.80±0.09和0.96±0.16比0.63 ±0.14,均P＜0.01),B組和C組蛋白錶達差異也有統計學意義(P＜0.05).結論 COPD模型大鼠骨骼肌組織Atrogin-1錶達增彊,且TNF-α可使Atrogin-1錶達上調.
목적 연구만성조새성폐질병(COPD)모형대서골격기조직범소단백련접매Atrogin-1적표체,이급종류배사인자α(TNF-α)대기적영향,탐토COPD대서골격기위축적궤제.방법 30지SD대서안수궤수자표법분위대조조(A조)、COPD조(B조)화COPD+ TNF-α조(C조),매조10지,단순연훈법제성COPD대서동물모형,분리지장신기,B조화C조분별급여불함화함TNF-α( 10 μg/L)적부육액진행리체유양부육.실시정량취합매련반응(PCR)화단백질인적검측Atrogin-1 mRNA화단백적표체.결과 B조화C조Atrogin-1적mRNA표체분별위A조적(1.48 ±0.27)배화(2.05 ±0.44)배(균P＜0.01),동시C조명현고우B조(1.41±0.32배,P＜0.05).B조화C조Atrogin-1단백표체야명현고우A조(0.80±0.09화0.96±0.16비0.63 ±0.14,균P＜0.01),B조화C조단백표체차이야유통계학의의(P＜0.05).결론 COPD모형대서골격기조직Atrogin-1표체증강,차TNF-α가사Atrogin-1표체상조.
Objective To study the expression of skeletal muscle E3 ubiquitin ligases atrogin-1 and the effect of tumor necrosis factor-α(TNF-α) on muscular atrophy in rats with chronic obstructive pulmonary disease(COPD) and discuss the mechanism of muscular atrophy of COPD rats.Methods Thirty SD rats were randomly divided into a control group(group A),a COPD group(group B) and a COPD + TNF-α group(group C),with 10rats in each group.After COPD models were eslablished by passive cigarette smoking in group B and C,the extensor digitorium longus muscles(EDL) were dissected and isolated in vitro muscle incubation system with adequate oxygen supply.The EDL were protein levels were delcrmined by real-lime quantitative PCR and Western blol respectively.Results The expressions of the Atrogin-1 mRNA of the group B and the group C were(1.475±0.272)times and(2.048±0.441) times more than that of control group(all P ＜ 0.01),meanwhile the level of expressions of the Atrogin-1 mRNA of group C was significantly higher than that of group B(P ＜ 0.05).The level of Atrogin-1 protein in group B and C were distinctly higher than that in group A(0.803±0.090) and(0.965±0.160) vs(0.626±0.142),all P ＜ 0.01,and the difference between group B and C was significant(P ＜ 0.05).Conclusion Atrogin-1 level in skeletal muscle of COPD model increases,which can be enhanced by TNF-α.The level of Atrogin-1 prolein in group B and C were dislinctly higher than that in group A(0.803±0.090 and 0.965±0.160 vs 0.626±0.142,all P ＜0.0 1),and the difference between group B and C was significant(P ＜0.05).
