摘要
目的探讨过氧化物酶体增殖因子活化受体γ(PPARγ)配体罗格列酮对肺腺癌A549细胞粘附分子整合素β1表达的影响及其作用机制。方法用逆转录-聚合酶联反应(RT-PCR)和间接免疫荧光标记流式细胞仪分别测定罗格列酮对A549细胞PPARγ、整合素β1 mRNA和蛋白表达的影响。结果罗格列酮激动A549细胞PPARγ的表达,抑制整合素β1的mRNA及蛋白的表达,呈剂量依赖关系。用PPARγ阻断剂GW9662,可取消其对整合素β1的抑制作用(P<0.05),用丝裂原激活蛋白激酶(MAPK)信号通路ERK抑制剂PD98059,可取消PPARγ对整合素β1的表达调控(P<0.05)。结论罗格列酮活化PPARγ抑制整合素β1的表达,丝裂原激活蛋白激酶(MAPK)信号通路参与此过程。
Aim To investigate the molecular mechanism of Rosiglitazone on the expression of integrin β1 in lung pulmonary carcinoma A549 cell line. Methods RT-PCR and flow cytometry methods were used to examine the expression of mRNA and cell total protein of PPARγ and integrin β1 subunit. Results The expres sion of PPARγ mRNA and integrin β1 mRNA had dose-dependent regulating action by Rosiglitazone, using PPARγ inhibitor GW9662 and ERK pathway inhibitor PD98059 could abolish the inhibition of PPARγ on the expression of integrin β1. Conclusion The effect of PPARγ ligand Rosiglitazone on integrin β1 expression is mediated through PPARγ-dependent signaling parthway. The mechanism may be partly involved in ERK pathway.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2007年第2期264-267,共4页
Chinese Pharmacological Bulletin
关键词
肺肿瘤
罗格列酮
整合素Β1
lung pulmonary carcinoma
rosiglitazone
integrin β1
