CAJ | 학술논문

目的探讨慢性阻塞性肺疾病(COPD)大鼠的气道重构与高迁移率族蛋白B1(HMGB1)表达水平的相关性.方法将健康无特定病原体(SPF)级Wistar雄性大鼠48只分为3组,每组16只.生理盐水对照组(A组)16只:于第1、14天在无菌操作下行颈前气管穿刺术,向气管内注入无菌注射用水0.2ml;COPD模型组(B组)16只:第1、14天向气管内注入脂多糖(LPS)200 μg(200 μl),第2～13、15 ～ 28天每天置于自制的烟熏箱内进行被动吸烟,每次10支,每天2次,每次持续60 min,连续28 d;断烟组(C组)16只:第1、14天向气道内注入LPS溶液200 μg(200 μl),第2～13、15～ 21天每天置于自制的烟熏箱内进行被动吸烟,每次10支,每天2次,每次持续60 min,连续21 d,实验最后1周断烟正常饲养.造模结束后观察各组大鼠气道炎症、气道重构及肺组织的病理改变,Western blot检测3组肺组织HMGB1蛋白的表达.结果 (1)B、C组气道重构指标细支气管管壁厚度与气管外径比值(MT,％)(B组9.21±3.54、C组8.23±3.32)、管壁面积与气管总面积比值(MA,％)(B组20.25±3.23、C组17.44±2.57)与A组[MT(4.62±2.58)％、MA(10.72±1.12)％]比较均明显增高(P＜0.05),C组较B组比较降低(P＜0.05).(2) Western blot结果显示:B、C组HMGB1蛋白表达[B组(1.621±0.254)、C组(1.234±0.327)]与A组(0.462±0.581)比较明显增强(P＜0.05),C组较B组HMGB1蛋白表达减弱(P＜0.05).结论 COPD疾病进展出现气道重构,且HMGB1的表达增强,说明HMGB1的表达可能与COPD的气道重构有关.
목적 탐토만성조새성폐질병(COPD)대서적기도중구여고천이솔족단백B1(HMGB1)표체수평적상관성.방법 장건강무특정병원체(SPF)급Wistar웅성대서48지분위3조,매조16지.생리염수대조조(A조)16지:우제1、14천재무균조작하행경전기관천자술,향기관내주입무균주사용수0.2ml;COPD모형조(B조)16지:제1、14천향기관내주입지다당(LPS)200 μg(200 μl),제2～13、15 ～ 28천매천치우자제적연훈상내진행피동흡연,매차10지,매천2차,매차지속60 min,련속28 d;단연조(C조)16지:제1、14천향기도내주입LPS용액200 μg(200 μl),제2～13、15～ 21천매천치우자제적연훈상내진행피동흡연,매차10지,매천2차,매차지속60 min,련속21 d,실험최후1주단연정상사양.조모결속후관찰각조대서기도염증、기도중구급폐조직적병리개변,Western blot검측3조폐조직HMGB1단백적표체.결과 (1)B、C조기도중구지표세지기관관벽후도여기관외경비치(MT,％)(B조9.21±3.54、C조8.23±3.32)、관벽면적여기관총면적비치(MA,％)(B조20.25±3.23、C조17.44±2.57)여A조[MT(4.62±2.58)％、MA(10.72±1.12)％]비교균명현증고(P＜0.05),C조교B조비교강저(P＜0.05).(2) Western blot결과현시:B、C조HMGB1단백표체[B조(1.621±0.254)、C조(1.234±0.327)]여A조(0.462±0.581)비교명현증강(P＜0.05),C조교B조HMGB1단백표체감약(P＜0.05).결론 COPD질병진전출현기도중구,차HMGB1적표체증강,설명HMGB1적표체가능여COPD적기도중구유관.
Objective To study the chronic obstructive pulmonary disease (COPD) in rat airway remodeling and high mobility group protein B1 (HMGB1) expression level of correlation.Methods Healthy specific pathogen free (SPF) level 48 Wistar male rats,divided into 3 groups,16 rats in each group.Normal saline control group (group A):in 1st,14 d in aseptic operation down neck trachea puncture,to intratracheal injection sterile water for injection 0.2 ml; COPD model group (group B):1st,14d anisotropic intratracheal injection of lipopolysaccharide (LPS) 200 μg (200 μl),2-13 d,15-28 d every day in self-made smoked is passive smoking,2 times a day,10 cigarettes each time,each lasting 60 min,continuous 28 d; smoking cessation group (group C) 16:in 1st,14 days to the airway is injected LPS solution 200 μg (200 μ1),2-13 d,15-21 d every day in self-made smoked is passive smoking,2 times a day,10 cigarettes each time,each lasting 60 min,continuous 21 d,the last 1 weeks of normal feeding experiments of broken smoke.Observing the pathological changes of rat airway inflammation,airway remodeling and pulmonary tissue after model establishment,with the expression of HMGB1 protein Western in lung tissue of three groups of blot detection.Results The group B,C of airway remodeling index fine bronchial wall thickness and pipe diameter ratio (MT,％) [group B (9.21 ± 3.54),group C (8.23 ± 3.32)],the Guan Bi area and tracheal total area ratio (MA％) [group B (20.25 ± 3.23),group C (17.44 ± 2.57)] and group A [MT,％ (4.62 ± 2.58),MA,％ (10.72 ± 1.12)] were significantly increased (P ＜ 0.05),compared with C group lower than group B (P ＜ 0.05).The Western blot electrophoresis showed that the expression of B and HMGB1 protein levels in group C [group B (1.621 ± 0.254),group C (1.234 ±0.327)] compared with group A (0.462 ±0.581) (P ＜0.05),significantly enhanced expression of group C than in group B decreased HMGB1 protein (P ＜ 0.05).Conclusion With the COPD disease progression of airway remodeling and the expression of HMGB1,enhance the expression of COPD and HMGB1,illustrate the airway remodeling related.