南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2014年
11期
1693-1696,1701
,共5页
HeLa细胞%曲格列酮%PPARγ%ICAM-1%MMP-9
HeLa細胞%麯格列酮%PPARγ%ICAM-1%MMP-9
HeLa세포%곡격렬동%PPARγ%ICAM-1%MMP-9
HeLa cells%troglitazone%proliferator-activated receptor-γ%intercellular adhesion molecule-1%matrix metalloprote-ainse-9
目的：探讨PPARγ激动剂曲格列酮对于宫颈癌HeLa细胞增殖及ICAM-1和MMP-9表达的影响。方法使用曲格列酮和/或GW9662（PPARγ拮抗剂）对HeLa细胞进行干预。在不同时间点（0、24、48和72 h）使用MTT法对HeLa细胞活性进行测定。在干预48 h后，使用RT-PCR和western blot对HeLa细胞ICAM-1、MMP-9和PPARγmRNA和蛋白进行测定。并使用EMSA对HeLa细胞PPARγDNA结合能力（核转录水平）进行分析。结果 GW9662组、曲格列酮+GW9662组与空白对照组相比较各时间点细胞活性未见显著统计学差异（P>0.05）；但曲格列酮组与空白对照组相比较细胞活性呈时间依赖性降低，差异有显著统计学意义（P均<0.05）。干预48 h后，曲格列酮组ICAM-1和MMP-9 mRNA和蛋白表达较空白对照组明显降低（P均<0.05）；但GW9662组和曲格列酮+GW9662组ICAM-1和MMP-9 mRNA和蛋白表达水平与空白对照组比较未见显著统计学差异（P均>0.05）。曲格列酮干预后HeLa细胞PPARγmRNA和蛋白表达水平和PPARγ核转位水平均显著增加，差异有显著统计学意义（P均<0.05）。结论本实验表明曲格列酮可以通过促进PPARγ表达和PPARγ的核转录水平下调HeLa细胞ICAM-1和MMP-9的合成，抑制HeLa细胞的增殖。
目的：探討PPARγ激動劑麯格列酮對于宮頸癌HeLa細胞增殖及ICAM-1和MMP-9錶達的影響。方法使用麯格列酮和/或GW9662（PPARγ拮抗劑）對HeLa細胞進行榦預。在不同時間點（0、24、48和72 h）使用MTT法對HeLa細胞活性進行測定。在榦預48 h後，使用RT-PCR和western blot對HeLa細胞ICAM-1、MMP-9和PPARγmRNA和蛋白進行測定。併使用EMSA對HeLa細胞PPARγDNA結閤能力（覈轉錄水平）進行分析。結果 GW9662組、麯格列酮+GW9662組與空白對照組相比較各時間點細胞活性未見顯著統計學差異（P>0.05）；但麯格列酮組與空白對照組相比較細胞活性呈時間依賴性降低，差異有顯著統計學意義（P均<0.05）。榦預48 h後，麯格列酮組ICAM-1和MMP-9 mRNA和蛋白錶達較空白對照組明顯降低（P均<0.05）；但GW9662組和麯格列酮+GW9662組ICAM-1和MMP-9 mRNA和蛋白錶達水平與空白對照組比較未見顯著統計學差異（P均>0.05）。麯格列酮榦預後HeLa細胞PPARγmRNA和蛋白錶達水平和PPARγ覈轉位水平均顯著增加，差異有顯著統計學意義（P均<0.05）。結論本實驗錶明麯格列酮可以通過促進PPARγ錶達和PPARγ的覈轉錄水平下調HeLa細胞ICAM-1和MMP-9的閤成，抑製HeLa細胞的增殖。
목적：탐토PPARγ격동제곡격렬동대우궁경암HeLa세포증식급ICAM-1화MMP-9표체적영향。방법사용곡격렬동화/혹GW9662（PPARγ길항제）대HeLa세포진행간예。재불동시간점（0、24、48화72 h）사용MTT법대HeLa세포활성진행측정。재간예48 h후，사용RT-PCR화western blot대HeLa세포ICAM-1、MMP-9화PPARγmRNA화단백진행측정。병사용EMSA대HeLa세포PPARγDNA결합능력（핵전록수평）진행분석。결과 GW9662조、곡격렬동+GW9662조여공백대조조상비교각시간점세포활성미견현저통계학차이（P>0.05）；단곡격렬동조여공백대조조상비교세포활성정시간의뢰성강저，차이유현저통계학의의（P균<0.05）。간예48 h후，곡격렬동조ICAM-1화MMP-9 mRNA화단백표체교공백대조조명현강저（P균<0.05）；단GW9662조화곡격렬동+GW9662조ICAM-1화MMP-9 mRNA화단백표체수평여공백대조조비교미견현저통계학차이（P균>0.05）。곡격렬동간예후HeLa세포PPARγmRNA화단백표체수평화PPARγ핵전위수평균현저증가，차이유현저통계학의의（P균<0.05）。결론본실험표명곡격렬동가이통과촉진PPARγ표체화PPARγ적핵전록수평하조HeLa세포ICAM-1화MMP-9적합성，억제HeLa세포적증식。
Objective To investigate the effect of troglitazone, a proliferator-activated receptor-γ (PPARγ) agonist, on the expressions of intercellular adhesion molecule-1 (ICAM-1) and matrix metalloproteainse-9 (MMP-9) and cell proliferation in HeLa cells. Methods MTT assay was used to measure the cell viability at different time points (0, 24, 48 and 72 h) after exposure to troglitazone. RT-PCR and Western blotting were employed to detect the mRNA and protein expressions of ICAM-1, MMP-9 and PPARγin the cells. Electrophoretic mobility shift assay (EMSA) was performed to assess the changes in DNA binding activity of PPARγ. Results The viability of HeLa cells were time-dependently inhibited by troglitazone, which also significantly reduced the mRNA and protein expressions of ICAM-1 and MMP-9 and increased PPARγexpression. The effects of troglitazone in inhibiting the cell viability and reducing ICAM-1 and MMP-9 expressions were antagonized by the application of the PPARγantagonist GW9662. The result of EMSA also showed significantly increased DNA binding activity of PPARγin the cells exposed to troglitazone. Conclusions The PPARγagonist troglitazone can inhibit the expression of ICAM-1 and MMP-9 in HeLa cells by up-regulating PPARγ.
