浙江医学
浙江醫學
절강의학
ZHEJIANG MEDICAL JOURNAL
2014年
13期
1133-1136
,共4页
吴立琴%戴元荣%李凤琴%王瑞丽%曾潍贤
吳立琴%戴元榮%李鳳琴%王瑞麗%曾濰賢
오립금%대원영%리봉금%왕서려%증유현
转化生长因子- β1%哮喘%气道平滑肌细胞%微囊蛋白- 1%ERK
轉化生長因子- β1%哮喘%氣道平滑肌細胞%微囊蛋白- 1%ERK
전화생장인자- β1%효천%기도평활기세포%미낭단백- 1%ERK
TGF- β1%Asthma%ASMC C%aveolin- 1%ERK
目的：探究TGF-β1对哮喘大鼠气道平滑肌细胞（ASMC）增殖的影响，进一步揭示哮喘的发病机制。方法建立大鼠慢性哮喘模型，原代分离培养大鼠ASMC，将细胞分为正常组、哮喘组、TGF-β1组和TGF-β1+PD-98059组，以CCK-8法检测细胞增殖，Western blot法检测caveolin-1和p- ERK1/2蛋白表达。结果 TGF-β1组细胞增殖较正常组和哮喘组明显（均P＜0.01）；TGF-β1+PD-98059组细胞增殖较TGF-β1组减低，但较哮喘组仍明显（均P＜0.05）。TGF-β1组p- ERK1/2表达量较正常组和哮喘组增加；TGF-β1+PD-98059组p- ERK1/2表达量较TGF-β1组减少，但较哮喘组表达量仍有所增加（均P＜0.05）。TGF-β1组caveolin-1表达量较正常组和哮喘组减少（均P＜0.05）；TGF-β1+PD-98059组caveolin-1表达量较TGF-β1组增加（P＜0.05）。结论 TGF-β1可以下调caveolin-1蛋白的表达量，激活ERK通路，从而促进哮喘大鼠ASMC的增殖，引起气道重塑。
目的：探究TGF-β1對哮喘大鼠氣道平滑肌細胞（ASMC）增殖的影響，進一步揭示哮喘的髮病機製。方法建立大鼠慢性哮喘模型，原代分離培養大鼠ASMC，將細胞分為正常組、哮喘組、TGF-β1組和TGF-β1+PD-98059組，以CCK-8法檢測細胞增殖，Western blot法檢測caveolin-1和p- ERK1/2蛋白錶達。結果 TGF-β1組細胞增殖較正常組和哮喘組明顯（均P＜0.01）；TGF-β1+PD-98059組細胞增殖較TGF-β1組減低，但較哮喘組仍明顯（均P＜0.05）。TGF-β1組p- ERK1/2錶達量較正常組和哮喘組增加；TGF-β1+PD-98059組p- ERK1/2錶達量較TGF-β1組減少，但較哮喘組錶達量仍有所增加（均P＜0.05）。TGF-β1組caveolin-1錶達量較正常組和哮喘組減少（均P＜0.05）；TGF-β1+PD-98059組caveolin-1錶達量較TGF-β1組增加（P＜0.05）。結論 TGF-β1可以下調caveolin-1蛋白的錶達量，激活ERK通路，從而促進哮喘大鼠ASMC的增殖，引起氣道重塑。
목적：탐구TGF-β1대효천대서기도평활기세포（ASMC）증식적영향，진일보게시효천적발병궤제。방법건립대서만성효천모형，원대분리배양대서ASMC，장세포분위정상조、효천조、TGF-β1조화TGF-β1+PD-98059조，이CCK-8법검측세포증식，Western blot법검측caveolin-1화p- ERK1/2단백표체。결과 TGF-β1조세포증식교정상조화효천조명현（균P＜0.01）；TGF-β1+PD-98059조세포증식교TGF-β1조감저，단교효천조잉명현（균P＜0.05）。TGF-β1조p- ERK1/2표체량교정상조화효천조증가；TGF-β1+PD-98059조p- ERK1/2표체량교TGF-β1조감소，단교효천조표체량잉유소증가（균P＜0.05）。TGF-β1조caveolin-1표체량교정상조화효천조감소（균P＜0.05）；TGF-β1+PD-98059조caveolin-1표체량교TGF-β1조증가（P＜0.05）。결론 TGF-β1가이하조caveolin-1단백적표체량，격활ERK통로，종이촉진효천대서ASMC적증식，인기기도중소。
Objective To investigate the effect of TGF- β1 on the proliferation of airway smooth muscle cells (ASMCs) in asthma rats. Methods Chronic asthma model was induced in rats and airway smooth muscle cells were isolated and cultured in vitro. The cultured ASMCs were divided into normal group, asthma group, TGF- β1 group and TGF- β1+PD- 98059 group. The cellproliferation was determined with CCK- 8 method and the expression of caveolin- 1 and p- ERK1/2 protein was detected with Western blot. Results The expression of p- ERK1/2 increased significantly in TGF- β1 group compared with other 3 groups (P<0.05), while the expression in TGF- β1+PD- 98059 group was higher than that in asthma group (P<0.05). The expression of caveolin- 1 in TGF- β1 group was lower than that in the normal group and asthma group as wel as in TGF- β1+PD- 98059 group (P<0.05). Conclusion TGF- β1 can down- regulate the expression of protein caveolin- 1 to activate the ERK pathway, thereby to promote the proliferation of airway smooth muscle cells, which final y causes airway remodeling.
