罗格列酮对肝癌SMMC-7721细胞VEGF蛋白表达的影响

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Akt_1/2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。

Effect of Rosiglitazone on Expression of VEGF in Liver Cancer Cell Line SMMC-7721

Objective To study the effects of rosiglitazone ligands of peroxisome proliferator-activated re-ceptor-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 100 μmol/L) for different time(24 h, 48 h and 72 h), the expressions of VEGF,PTEN, Akt_(1/2) and P-Akt_1 were detected by western blot. Results Rosiglitazone could signifi-cantly inhibit the expression of VEGF in SMMC-7721 cells and have both time-dependent and concentra-tion-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 Akt_(1/2) and P-Akt_1. Conclusion This study suggested that activation of PPARγ by rosiglitazone can in-hibit the expression of VEGF, which may be through the upregulation the expression level of PTEN while not directly relying on PI3K/Akt.