罗格列酮上调PPARγ抑制舌癌Tca8113细胞VEGF表达的实验研究  

Rosiglitazone inhibits VEGF expression by up-regulation of PPARγin tongue cancer Tca8113 cells

作　　者：于四海[1] 严晓峰[1] 

机构地区：[1]重庆市公共卫生医疗救治中心口腔科,重庆400036

出　　处：《西部医学》2015年第7期967-970,共4页Medical Journal of West China

基　　金：国家"十二五"科技重大专项课题(2012zx10005-008)

摘　　要：目的探讨过氧化物酶体增殖物激活受体γ(PPARγ)激动剂罗格列酮(rosiglitazone)对于舌癌Tca8113细胞VEGF表达的调节作用。方法将Tca8113细胞分为对照组(Control组)、罗格列酮干预组(ROS组)及罗格列酮+PPARγ抑制剂GW9662组(ROS+GW组)共三组。使用MTT法对不同时间点(0、24、72h)的Tca8113细胞活性进行检测;使用western blot法对干预24小时后Tca8113细胞PPARγ及VEGF的活化水平进行分析。结果与对照组相比,罗格列酮干预的Tca8113细胞活性呈时间依赖性下降,差异均有显著统计学意义(P<0.05),且各时间点ROS组较ROS+GW组细胞活性下降程度更加明显,差异均有显著统计学意义(P<0.05)。干预24小时后,罗格列酮干预的Tca8113细胞PPARγ表达水平显著增加,VEGF表达水平显著降低,差异有显著统计学意义(P<0.05);且ROS组较ROS+GW组细胞PPARγ表达增加及VEGF表达降低更加明显,差异有显著统计学意义(P<0.05)。结论罗格列酮可以通过上调PPARγ抑制人舌鳞状细胞癌Tca8113细胞VEGF表达,从而抑制Tca8113细胞的增殖。该实验为PPARγ激动剂罗格列酮应用于肿瘤的临床治疗提供了理论依据。Objective To explore the effect of rosiglitazone on the expression of VEGF in tongue cancer Tca8113 cells,and its potential mechanism.Methods Tca8113 cells were separated into 3groups,Control group,Rosiglitazone（ROS）group and Rosiglitazone＋GW9662group（ROS＋GW group）.The cell viabilities of Tca8113 cells in different time points（0h,24 hand 72h）were measured by MTT.After 24 hours treatments,the expression of PPARγand VEGF were detected by western blot.Results The cell viabilities of Tca8113 cells were time-dependently inhibited by rosiglitazone administration.Moreover,GW9662 abrogated this value of rosiglitazone.After 24 hours treatments,the expression of PPARγwas significantly increased and the expression of VEGF was largely reduced.Nevertheless,our data also showed that these effects of rosiglitazone were significantly blunted by PPARγantagonist GW9662 in Tca8113cells.Conclusions Rosiglitazone could reduce the proliferation and inhibit the expression of VEGF by up-regulation of PPARγin tongue cancer Tca8113 cells.

关 键 词：TCA8113细胞 罗格列酮 过氧化物酶体增殖物激活受体Γ 血管内皮生长因子 

分 类 号：R739.86[医药卫生—肿瘤]