CAJ | 학술논문

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·mL-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-qPCR）检测和比较其 PPARγ mRNA 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5 ng·mL-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）。PPARγ mRNA 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。
목적：연구필격렬동대인위암 SGC7901세포주체외생장적영향。방법채용5 ng·mL-1 TGF-β1유도위암SGC7901세포24 h 후，급여불동농도（0、5、10、20、40μmol·L-1）필격렬동처리불동시간（0、12、24、48、72 h），분별채용MTT 법화류식세포술검측세포증식화세포조망정황，동시채용실시형광정량취합매련반응기술（RT-qPCR）검측화비교기 PPARγ mRNA 적표체수평。결과재5～40μmol·L-1적농도범위내，필격렬동이제량화시간의뢰성방식억제5 ng·mL-1적 TGF-β1유도적위암 SGC7901세포증식（P<0.05）。10μmol·L-1필격렬동처리인위암 SGC7901세포12 h，기조망솔교대조조현저승고，병수기작용농도적승고화시간적연장축점승고，72 h 시최고（P<0.01）。PPARγ mRNA 표체수평수착필격렬동농도적증가화작용시간적연장이축점상조，차이교정상조구유통계학의의（P<0.05）。결론필격렬동가능통과상조 PPARγ적표체이제량화시간의뢰성방식억제 TGF-β1유도적인위암 SGC7901세포적생장，병촉진기조망。
Objectives To research the effects of pioglitazone on SGC7901 human gastric cancer cell line. Methods After induced by 5 ng·mL-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 real-time fluorescent quantitative polymerase chain reaction (RT-qPCR) was applied to detect the gene expression level of peroxisome proliferator-activated receptorγ (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-1 of pioglitazone for 12 h, the apoptosis rate of TGF-β1 induced SGC7901 cell was increased significantly as compared with the con-trol 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 PPARγmRNA expression level was also gradually upregulated along with the increase of the concentration of pioglitazone and treat-ing time, and difference had statistical significance (P<0.05). Conclusion Pioglitazone could inhibit the growth and promote the ap-optosis of TGF-β1 induced gastric cancer SGC7901 cells in a dose and time dependent manner through upregulating the expression of the PPARγ.