吡格列酮对人胃癌SGC7901细胞增殖和凋亡的影响

Effects of Pioglitazone on the Proliferation and Apoptosis of Human Gastric Cancer Cell Line SGC7901

目的研究吡格列酮对人胃癌SGC7901细胞株体外生长的影响。方法采用5 ng·m L^-1 TGF-β1诱导胃癌SGC7901细胞24 h后,给予不同浓度（0、5、10、20、40μmol·L^-1）吡格列酮处理不同时间（0、12、24、48、72 h）,分别采用MTT法和流式细胞术检测细胞增殖和细胞凋亡情况,同时采用实时荧光定量聚合酶链反应技术（RT-q PCR）检测和比较其PPARγm RNA的表达水平。结果在5-40μmol·L-^1的浓度范围内,吡格列酮以剂量和时间依赖性方式抑制5ng·m L^-1的TGF-β1诱导的胃癌SGC7901细胞增殖（P〈0.05）。10μmol·L-1吡格列酮处理人胃癌SGC7901细胞12 h,其凋亡率较对照组显著升高,并随其作用浓度的升高和时间的延长逐渐升高,72 h时最高（P〈0.01）。PPARγm RNA表达水平随着吡格列酮浓度的增加和作用时间的延长而逐渐上调,差异较正常组具有统计学意义（P〈0.05）。结论吡格列酮可能通过上调PPARγ的表达以剂量和时间依赖性方式抑制TGF-β1诱导的人胃癌SGC7901细胞的生长,并促进其凋亡。

Objectives To research the effects of pioglitazone on SGC7901 human gastric cancer cell line. Methods After induced by 5 ng·m L^-1 TGF-β1, the SGC7901 human gastric cancer cell line in the research groups were treated by pioglitazone with different concentrations（5, 10, 20, 25 μmol·L^-1） for different times（0, 12, 24, 48, 72 h）. The control group had no medicament of pioglitazone. Then the proliferation and apoptosis of gastric cancer cells was detected respectively by MTT and flow cytometry method. The realtime fluorescent quantitative polymerase chain reaction（RT-q PCR） was applied to detect the gene expression level of peroxisome proliferator-activated receptor γ（PPARγ）. Results Within the concentration range of 5-40 μmol·L^-1, pioglitazone inhibited the growth of 5 ng·ml^-1 TGF-β1 induced SGC7901 cells in a dose and time dependent manner（P〈0.05）. After treated by 10 μmol·L^-1of pioglitazone for 12 h, the apoptosis rate of TGF-β1 induced SGC7901 cell was increased significantly as compared with the control group, and it was increased gradually along with the increase of the dose and time and reached the highest at 72 h（P〈0.01）. The PPARγ m RNA expression level was also gradually upregulated along with the increase of the concentration of pioglitazone and treating time, and difference had statistical significance（P〈0.05）. Conclusion Pioglitazone could inhibit the growth and promote the apoptosis of TGF-β1 induced gastric cancer SGC7901 cells in a dose and time dependent manner through upregulating the expression of the PPARγ.