中华生物医学工程杂志
中華生物醫學工程雜誌
중화생물의학공정잡지
CHINESE JOURNAL OF BIOMEDICAL ENGINEERING
2012年
1期
6-10
,共5页
邹威凤%胡国平%李冰%冉丕鑫
鄒威鳳%鬍國平%李冰%冉丕鑫
추위봉%호국평%리빙%염비흠
肺疾病,慢性阻塞性%Wnt蛋白质类%Wnt-β-catenin信号途径%气道重构%香烟烟雾%大鼠
肺疾病,慢性阻塞性%Wnt蛋白質類%Wnt-β-catenin信號途徑%氣道重構%香煙煙霧%大鼠
폐질병,만성조새성%Wnt단백질류%Wnt-β-catenin신호도경%기도중구%향연연무%대서
Pulmonary disease,chronic obstructive%Wnt proteins%Wnt-β-catenin signaling pathway%Airway remodeling%Cigarette smoke%Rats
目的 探讨香烟烟雾暴露对大鼠肺组织Wnt3a和β-catenin蛋白表达的影响.方法 20只雌性SD大鼠,按随机数字表分为对照组和模型组,每组10只.模型组大鼠被动吸入香烟烟雾,每天2次,每次45 min；对照组大鼠不接触香烟烟雾.100d后处死动物,光镜下观察肺组织的病理形态学改变,免疫组化法检测肺组织α-平滑肌肌动蛋白(α-SMA)、Wnt3a和β-catenin蛋白表达,并测定2组大鼠支气管平滑肌厚度.结果 模型组大鼠肺组织呈现慢性炎性反应和肺气肿样改变,小气道壁及平滑肌层增厚明显.α-SMA主要表达于气道和血管的平滑肌层.模型组支气管平滑肌厚度高于对照组[ (3.06±0.62) μm比(1.86±0.43) μm,P＜0.05].Wnt3a和β-catenin主要表达于支气管上皮细胞和肺泡上皮细胞.模型组与对照组支气管上皮细胞Wnt3a蛋白表达分别为74.54±4.14、89.24±3.02；肺泡上皮细胞Wnt3a蛋白表达分别为91.97±2.50、110.46±3.85,组间比较差异均有统计学意义(均P＜0.05).模型组与对照组支气管上皮细胞胞质β-catenin蛋白表达分别为86.97±4.87、103.18±3.77;支气管上皮细胞胞核β-catenin蛋白表达分别为95.75±3.91、116.12±5.76;肺泡上皮细胞胞质β-catenin蛋白表达分别为106.24±4.57、128.81±3.96；肺泡上皮细胞胞核β-catenin蛋白表达分别为125.44±4.89、152.90±4.10,组间比较差异均有统计学意义(均P＜0.05).结论 香烟烟雾可诱导大鼠肺组织Wnt3a和β-catenin蛋白表达上调.
目的 探討香煙煙霧暴露對大鼠肺組織Wnt3a和β-catenin蛋白錶達的影響.方法 20隻雌性SD大鼠,按隨機數字錶分為對照組和模型組,每組10隻.模型組大鼠被動吸入香煙煙霧,每天2次,每次45 min；對照組大鼠不接觸香煙煙霧.100d後處死動物,光鏡下觀察肺組織的病理形態學改變,免疫組化法檢測肺組織α-平滑肌肌動蛋白(α-SMA)、Wnt3a和β-catenin蛋白錶達,併測定2組大鼠支氣管平滑肌厚度.結果 模型組大鼠肺組織呈現慢性炎性反應和肺氣腫樣改變,小氣道壁及平滑肌層增厚明顯.α-SMA主要錶達于氣道和血管的平滑肌層.模型組支氣管平滑肌厚度高于對照組[ (3.06±0.62) μm比(1.86±0.43) μm,P＜0.05].Wnt3a和β-catenin主要錶達于支氣管上皮細胞和肺泡上皮細胞.模型組與對照組支氣管上皮細胞Wnt3a蛋白錶達分彆為74.54±4.14、89.24±3.02；肺泡上皮細胞Wnt3a蛋白錶達分彆為91.97±2.50、110.46±3.85,組間比較差異均有統計學意義(均P＜0.05).模型組與對照組支氣管上皮細胞胞質β-catenin蛋白錶達分彆為86.97±4.87、103.18±3.77;支氣管上皮細胞胞覈β-catenin蛋白錶達分彆為95.75±3.91、116.12±5.76;肺泡上皮細胞胞質β-catenin蛋白錶達分彆為106.24±4.57、128.81±3.96；肺泡上皮細胞胞覈β-catenin蛋白錶達分彆為125.44±4.89、152.90±4.10,組間比較差異均有統計學意義(均P＜0.05).結論 香煙煙霧可誘導大鼠肺組織Wnt3a和β-catenin蛋白錶達上調.
목적 탐토향연연무폭로대대서폐조직Wnt3a화β-catenin단백표체적영향.방법 20지자성SD대서,안수궤수자표분위대조조화모형조,매조10지.모형조대서피동흡입향연연무,매천2차,매차45 min；대조조대서불접촉향연연무.100d후처사동물,광경하관찰폐조직적병리형태학개변,면역조화법검측폐조직α-평활기기동단백(α-SMA)、Wnt3a화β-catenin단백표체,병측정2조대서지기관평활기후도.결과 모형조대서폐조직정현만성염성반응화폐기종양개변,소기도벽급평활기층증후명현.α-SMA주요표체우기도화혈관적평활기층.모형조지기관평활기후도고우대조조[ (3.06±0.62) μm비(1.86±0.43) μm,P＜0.05].Wnt3a화β-catenin주요표체우지기관상피세포화폐포상피세포.모형조여대조조지기관상피세포Wnt3a단백표체분별위74.54±4.14、89.24±3.02；폐포상피세포Wnt3a단백표체분별위91.97±2.50、110.46±3.85,조간비교차이균유통계학의의(균P＜0.05).모형조여대조조지기관상피세포포질β-catenin단백표체분별위86.97±4.87、103.18±3.77;지기관상피세포포핵β-catenin단백표체분별위95.75±3.91、116.12±5.76;폐포상피세포포질β-catenin단백표체분별위106.24±4.57、128.81±3.96；폐포상피세포포핵β-catenin단백표체분별위125.44±4.89、152.90±4.10,조간비교차이균유통계학의의(균P＜0.05).결론 향연연무가유도대서폐조직Wnt3a화β-catenin단백표체상조.
Objective To investigate the effects of cigarette smoke(CS) exposure on expression of Wnt3a and β-catenin protein in rat lung tissue.Methods Twenty female SD rats were allocated to 2 groups (n=10 each) by random digit table:the control group and CS exposure group(model group).Rats in model group were subjected to twice-daily 45-min CS exposure,while the rats in control group were kept isolated from CS.The animals were sacrificed on day 100 to be harvested for lung tissues which were then studied for pathological morphology under light microscopy,expressions of α-smooth muscle actin (α-SMA),Wnt3a and β-catenin proteins by immunohistochemistry, and thickness of bronchial smooth muscle layer by morphometry.Results The rats in model group showed chronic inflammation,emphysema-like change and thickening of small airway walls and smooth muscle layers in the lung tissues.In both groups,α-SMA protein was localized in the smooth muscle layer of airway and vessel.The mean thickness of bronchial smooth muscle was significantly greater in the model group than those in control group [ (3.06±0.62) μm vs ( 1.86±0.43) μm,P＜0.05].Wnt3a and β-catenin were mainly expressed in the bronchial and alveolar epithelium.In model group and control group,the levels of Wnt3a expression were 74.54 ±4.14 vs 89.24 ± 3.02 in bronchial epithelial cells,and 91.97 ± 2.50 vs 110.46 ± 3.85 in alveolar epithelial cells,with significant differences between groups (both P＜0.05) ; the levels of β-catenin expression were 86.97±4.87 vs 103.18±3.77 in cytoplasm of bronchial epithelial cells,and 95.75 ±3.91 vs 116.12±5.76 in nuclei of bronchial epithelial cells,106.24±4.57 vs 128.81±3.96 in cytoplasm of alveolar epithelial cells,and 125.44±4.89 vs 152.90±4.10 in nuclei of alveolar epithelial cells,with significant differences between groups (all P＜0.05).Conclusions Cigarette smoke may induce up-regulation of Wnt3a and β-catenin proteins in rat lung tissue.
