安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
ACTA UNIVERSITY MEDICINALIS ANHUI
2014年
7期
901-904,905
,共5页
黄传兵%万磊%刘健%李明%纵瑞凯%曹云祥%朱艳
黃傳兵%萬磊%劉健%李明%縱瑞凱%曹雲祥%硃豔
황전병%만뢰%류건%리명%종서개%조운상%주염
佐剂性关节炎%心功能%肺功能%Smad通路%转化生长因子
佐劑性關節炎%心功能%肺功能%Smad通路%轉化生長因子
좌제성관절염%심공능%폐공능%Smad통로%전화생장인자
adjuvant arthritis%cardiac function%pulmonary function%Smad pathway%transforming growth factor
目的:研究佐剂性关节炎( AA)大鼠心肺功能变化与转化生长因子β1( TGF-β1)/Smad2、4、7通路的关系。方法将30只大鼠随机均分为正常对照组和模型组,向模型组大鼠右后足跖皮内注射弗氏完全佐剂0.1 ml致炎,复制成AA模型。致炎19 d后,观察大鼠足跖肿胀度、关节炎指数( AI),采用超声诊断仪检测大鼠心功能、小动物肺功能仪检测肺功能变化,免疫印迹法检测大鼠心肺 TGF-β1、Smad2、Smad4、Smad7蛋白表达。结果与正常对照组比较,模型组大鼠足趾肿胀度、AI 升高,心肺功能降低,心肺组织 TGF-β1、Smad2、Smad4蛋白表达升高,Smad7降低( P<0.01,P<0.05);相关性分析显示,足趾肿胀度与75%肺活量的最大呼气流量(FEF75)呈负相关,AI与左房舒张末期内径(LA)呈正相关,与用力最大呼气流量( MFEF)呈负相关,TGF-β1与左心室短轴缩短率( FS )、50%肺活量的最大呼气流量( FEF50)呈负相关,Smad2与左室舒张末期内径( LV)呈正相关,Smad4与舒张早期峰值流速( E 峰)、FEF75呈负相关, Smad7与FEF75、MFEF呈正相关(P<0.01,P<0.05)。结论AA大鼠心肺功能损伤可能与TGF-β1/Smad2、4、7信号通路过度激活有关。
目的:研究佐劑性關節炎( AA)大鼠心肺功能變化與轉化生長因子β1( TGF-β1)/Smad2、4、7通路的關繫。方法將30隻大鼠隨機均分為正常對照組和模型組,嚮模型組大鼠右後足蹠皮內註射弗氏完全佐劑0.1 ml緻炎,複製成AA模型。緻炎19 d後,觀察大鼠足蹠腫脹度、關節炎指數( AI),採用超聲診斷儀檢測大鼠心功能、小動物肺功能儀檢測肺功能變化,免疫印跡法檢測大鼠心肺 TGF-β1、Smad2、Smad4、Smad7蛋白錶達。結果與正常對照組比較,模型組大鼠足趾腫脹度、AI 升高,心肺功能降低,心肺組織 TGF-β1、Smad2、Smad4蛋白錶達升高,Smad7降低( P<0.01,P<0.05);相關性分析顯示,足趾腫脹度與75%肺活量的最大呼氣流量(FEF75)呈負相關,AI與左房舒張末期內徑(LA)呈正相關,與用力最大呼氣流量( MFEF)呈負相關,TGF-β1與左心室短軸縮短率( FS )、50%肺活量的最大呼氣流量( FEF50)呈負相關,Smad2與左室舒張末期內徑( LV)呈正相關,Smad4與舒張早期峰值流速( E 峰)、FEF75呈負相關, Smad7與FEF75、MFEF呈正相關(P<0.01,P<0.05)。結論AA大鼠心肺功能損傷可能與TGF-β1/Smad2、4、7信號通路過度激活有關。
목적:연구좌제성관절염( AA)대서심폐공능변화여전화생장인자β1( TGF-β1)/Smad2、4、7통로적관계。방법장30지대서수궤균분위정상대조조화모형조,향모형조대서우후족척피내주사불씨완전좌제0.1 ml치염,복제성AA모형。치염19 d후,관찰대서족척종창도、관절염지수( AI),채용초성진단의검측대서심공능、소동물폐공능의검측폐공능변화,면역인적법검측대서심폐 TGF-β1、Smad2、Smad4、Smad7단백표체。결과여정상대조조비교,모형조대서족지종창도、AI 승고,심폐공능강저,심폐조직 TGF-β1、Smad2、Smad4단백표체승고,Smad7강저( P<0.01,P<0.05);상관성분석현시,족지종창도여75%폐활량적최대호기류량(FEF75)정부상관,AI여좌방서장말기내경(LA)정정상관,여용력최대호기류량( MFEF)정부상관,TGF-β1여좌심실단축축단솔( FS )、50%폐활량적최대호기류량( FEF50)정부상관,Smad2여좌실서장말기내경( LV)정정상관,Smad4여서장조기봉치류속( E 봉)、FEF75정부상관, Smad7여FEF75、MFEF정정상관(P<0.01,P<0.05)。결론AA대서심폐공능손상가능여TGF-β1/Smad2、4、7신호통로과도격활유관。
Objective To study the changes of cardiopulmonary function and transforming growth factor beta1 (TGF-β1)/Smad2, 4, 7 pathway in rats of adjuvant arthritis (AA). Methods Thirty rats were randomly divided into normal control group and model group. The model group was intracutaneously injected with 0. 1 ml of Freund’ s complete adjuvant in the right hindlimb. After nineteen days of inflammatory-induction, paw swelling and arthritis index ( AI) were observed cardiac function was tested using ultrasonic diagnostic, and pulmonary function was test-ed using small animal spirometer. The expressions of TGF-β1, Smad2, Smad4, Smad7 protein were detected by Western blot. Results Compared with normal control group, paw swelling, AI, TGF-β1, Smad2, Smad4 protein were increased, and cardiopulmonary function parameters, cardiopulmonary, Smad7 protein were decreased in rats of AA ( P<0. 01 , P<0. 05 ) . There were negative correlations between paw swelling and 75% of vital capacity maximum expiratory flow ( FEF75 ) , AI and maximum forced expiratory flow ( MFEF ) , TGF-β1 and fractional shortening ( FS) , 50% of vital capacity maximum expiratory flow ( FEF50 ) , Smad4 and peak early diastolic veloci-ty (E), FEF75(P<0. 01, P<0. 05). There were positive correlations between AI and left ventricular diastolic di-ameter (LV), Smad2 and left atrial diastolic diameter(LA), Smad7 and FEF75, MFEF (P<0. 01, P<0. 05). Conclusion Heart and lung function impairment may be associated with excessive activation in signaling pathways of TGF-β1/Smad2,4,7 in AA.