中华结核和呼吸杂志
中華結覈和呼吸雜誌
중화결핵화호흡잡지
Chinese Journal of Tuberculosis and Respiratory Diseases
2012年
5期
336-339
,共4页
王晓飞%丁辉%周凤秋%孟凡青%蔡后荣
王曉飛%丁輝%週鳳鞦%孟凡青%蔡後榮
왕효비%정휘%주봉추%맹범청%채후영
窖蛋白1%肺纤维化%Smad蛋白质类%肌动蛋白类%胶原
窖蛋白1%肺纖維化%Smad蛋白質類%肌動蛋白類%膠原
교단백1%폐섬유화%Smad단백질류%기동단백류%효원
Caveolin 1%Pulmonary fibrosis%Smad proteins%Actin%Collagen
目的 研究特发性肺纤维化(IPF)患者肺组织窖蛋白-1和细胞外基质表达的变化及其意义.方法 6例IPF患者的肺组织标本来自2005年1月至2008年12月南京大学医学院附属鼓楼医院呼吸科住院患者,其开胸肺活检组织病理诊断符合普通型间质性肺炎.6例肺癌患者行肺叶切除,取其远离病变的肺组织标本作为对照组.用RT-PCR、Western blot及免疫组织化学方法检测肺组织标本中的窖蛋白-1 mRNA和蛋白表达.Western blot检测肺组织标本的胶原-Ⅰ、α-平滑肌肌动蛋白(α-SMA)和Smads蛋白表达.结果 IPF患者肺组织窖蛋白-1的mRNA和蛋白表达(分别为0.05±0.02和0.16±0.05)明显低于对照组(分别为0.66±0.19和0.81±0.11),差异有统计学意义(F值分别为8.465和353.836,均P<0.05).IPF患者肺组织的胶原-Ⅰ (0.85±0.11)和α-SMA蛋白(0.78±0.08)表达明显高于对照组(分别为0.16±0.04和0.14±0.05),差异有统计学意义(F值分别为485.09、410.027,均P<0.05).IPF患者肺组织的p-Smad2蛋白(0.78±0.08)和p-Smad3蛋白(0.86±0.07)表达明显高于对照组(分别为0.17±0.04和0.14±0.04),差异有统计学意义(F值分别为521.97和530.48,均P<0.05);而Smad7蛋白表达(0.22±0.05)明显低于对照组(0.78±0.08),差异有统计学意义(F=414.84,P<0.05).结论 IPF患者肺组织窖蛋白-1表达下调与特发性肺纤维化的发生和发展有关.
目的 研究特髮性肺纖維化(IPF)患者肺組織窖蛋白-1和細胞外基質錶達的變化及其意義.方法 6例IPF患者的肺組織標本來自2005年1月至2008年12月南京大學醫學院附屬鼓樓醫院呼吸科住院患者,其開胸肺活檢組織病理診斷符閤普通型間質性肺炎.6例肺癌患者行肺葉切除,取其遠離病變的肺組織標本作為對照組.用RT-PCR、Western blot及免疫組織化學方法檢測肺組織標本中的窖蛋白-1 mRNA和蛋白錶達.Western blot檢測肺組織標本的膠原-Ⅰ、α-平滑肌肌動蛋白(α-SMA)和Smads蛋白錶達.結果 IPF患者肺組織窖蛋白-1的mRNA和蛋白錶達(分彆為0.05±0.02和0.16±0.05)明顯低于對照組(分彆為0.66±0.19和0.81±0.11),差異有統計學意義(F值分彆為8.465和353.836,均P<0.05).IPF患者肺組織的膠原-Ⅰ (0.85±0.11)和α-SMA蛋白(0.78±0.08)錶達明顯高于對照組(分彆為0.16±0.04和0.14±0.05),差異有統計學意義(F值分彆為485.09、410.027,均P<0.05).IPF患者肺組織的p-Smad2蛋白(0.78±0.08)和p-Smad3蛋白(0.86±0.07)錶達明顯高于對照組(分彆為0.17±0.04和0.14±0.04),差異有統計學意義(F值分彆為521.97和530.48,均P<0.05);而Smad7蛋白錶達(0.22±0.05)明顯低于對照組(0.78±0.08),差異有統計學意義(F=414.84,P<0.05).結論 IPF患者肺組織窖蛋白-1錶達下調與特髮性肺纖維化的髮生和髮展有關.
목적 연구특발성폐섬유화(IPF)환자폐조직교단백-1화세포외기질표체적변화급기의의.방법 6례IPF환자적폐조직표본래자2005년1월지2008년12월남경대학의학원부속고루의원호흡과주원환자,기개흉폐활검조직병리진단부합보통형간질성폐염.6례폐암환자행폐협절제,취기원리병변적폐조직표본작위대조조.용RT-PCR、Western blot급면역조직화학방법검측폐조직표본중적교단백-1 mRNA화단백표체.Western blot검측폐조직표본적효원-Ⅰ、α-평활기기동단백(α-SMA)화Smads단백표체.결과 IPF환자폐조직교단백-1적mRNA화단백표체(분별위0.05±0.02화0.16±0.05)명현저우대조조(분별위0.66±0.19화0.81±0.11),차이유통계학의의(F치분별위8.465화353.836,균P<0.05).IPF환자폐조직적효원-Ⅰ (0.85±0.11)화α-SMA단백(0.78±0.08)표체명현고우대조조(분별위0.16±0.04화0.14±0.05),차이유통계학의의(F치분별위485.09、410.027,균P<0.05).IPF환자폐조직적p-Smad2단백(0.78±0.08)화p-Smad3단백(0.86±0.07)표체명현고우대조조(분별위0.17±0.04화0.14±0.04),차이유통계학의의(F치분별위521.97화530.48,균P<0.05);이Smad7단백표체(0.22±0.05)명현저우대조조(0.78±0.08),차이유통계학의의(F=414.84,P<0.05).결론 IPF환자폐조직교단백-1표체하조여특발성폐섬유화적발생화발전유관.
Objective To investigate the expressions of caveolin-1,collagen- Ⅰ,α-smooth muscle actin(α-SMA) and Smad in lung tissues of patients with idiopathic pulmonary fibrosis (IPF) and therefore to explore their potential roles in the pathogenesis of the disease.Methods Six patients with IPF confirmed pathologically by open lung biopsy in Department of Pulmonary Medicine,Affiliated Drum Tower Hospital of Nanjing University from January 2005 to December 2008 were studied. Diagnosis of IPF was made in accordance with the American Thoracic Society/European Respiratory Society Consensus Statement.At the same period,6 normal lung samples were also obtained from patients with lung cancer by surgical resections as the control group.The level of caveolin-1 mRNA and protein,collagen- Ⅰ,α-SMA and Smads in lung tissues were detected by RT-PCR,Western blot and immunohistochemistry.Results Compared with the control group,significantly reduced levels of caveolin-1 mRNA and protein (0.66:±0.19 vs 0.05 ±0.02;0.81 ±0.11 vs 0.16 ±0.05,P <0.05) were observed in the lungs of patients with IPF.However,collagen-Ⅰ (0.85 ±0.11 vs 0.16 ± 0.04) and α-SMA(0.78 ±0.08 vs 0.14 ±0.05) proteins in the lung tissues of IPF patients were significantly increased as compared to the controls( P <0.05 ).The expressions of p-Smad2 and p-Smad3 proteins were significantly increased (0.78 ± 0.08 vs 0.17 ± 0.04 ;0.86 ± 0.07 vs 0.14 ± 0.04,respectively,P <0.05),while that of smad7 protein decreased (0.22 ±0.05 vs 0.78 ±0.08,P <0.05) in the lungs of patients with IPF as compared with the control groups.Conclusion The reduced expression of caveolin-1 in lung tissues of IPF may be related to the development and progress of pulmonary fibrosis.