【摘要】 目的探讨过氧化物酶体增殖激活物受体γ(PPARγ)配体罗格列酮对肝癌SMMC-7721细胞中VEGF表达的影响及其可能机制。方法经不同浓度罗格列酮(0、0.1、1、10、100μmol/L)分别作用SMMC-7721细胞24h、48h、72h后,采用Western印迹法检测细胞VEGF和PTEN、Akt1/2及P-Akt1蛋白表达的变化。结果罗格列酮可以显著抑制SMMC-7721细胞中VEGF蛋白表达水平(P<0.05),呈时间和剂量依赖性;能上调细胞PTEN的表达,并呈时间和剂量依赖性(P<0.05),但Akt1/2及P-Akt1的表达无明显改变(P>0.05)。结论罗格列酮可抑制SMMC-7721细胞中VEGF蛋白表达,该作用可能是与上调PTEN表达有关,但不是通过直接抑制PI3K/Akt信号转导途径来实现的。更多还原

【Abstract】 Objective To study the effects of rosiglitazone ligands of peroxisome proliferator-activated receptor-γ(PPAR-γ) on the expression of VEGF in hepatocellular carcinoma cell line SMMC-7721,in vitro and to reveal the related molecular mechanisms.Methods After treatment with different concentration of rosiglitazone (0,0.1,1,10 and 100μmol/L) for different time(24h,48h and 72h),the expressions of VEGF,PTEN,Akt1/2 and P-Akt1 were detected by western blot.Results Rosiglitazone could significantly inhibit the expression of VEGF in SMMC-7721 cells and have both time-dependent and concentration-dependent manner(P<0.05).Rosiglitazone increased the expression of PTEN remarkably in both time-dependent and concentration-dependent manner(P<0.05),but has no influence on the expression of Akt1/2 and P-Akt1.Conclusion This study suggested that activation of PPARγ by rosiglitazone can inhibit the expression of VEGF,which may be through the upregulation the expression level of PTEN while not directly relying on PI3K/Akt.更多还原