CAJ | 학술논문

目的研究PPARγ激动剂罗格列酮(RSG)与全反式维甲酸(ATRA)对人胃癌SGC7901细胞株生长和凋亡的影响及其机制的研究.方法体外培养SGC7901细胞,实验分为空白对照组、10μmol/L ATRA组、12.5 μmol/L RSG、25 μmol/L RSG组,10 μmol/L ATRA和25 μmol/L RSG联合组.MTT法检测细胞生长抑制率,流式细胞仪测定细胞周期,HE染色检测细胞形态,免疫细胞化学检测PPARγ蛋白,RT-PCR检测PPARγmRNA.结果 10 μmol/L ATRA、12.5 mmol/L RSG、25 mmol/L RSG及两药联合时皆可抑制SGC7901细胞的增殖,且存在浓度及时间依赖,两药联合作用72 h时,生长抑制率为(29.73±0.69)%.ATRA、RSG皆可使细胞周期G0/G1期延长,S期下降,两药联合作用时,S%为(12.87±0.35)%,细胞形态向正常方向转化,细胞的PPARγ蛋白核内表达及PPARγmRNA表达上调,两药联合后作用进一步加强,PPARγ/GAPDH的浓度比值高达0.646.结论 ATRA、RSG均可抑制SGC7901细胞增殖,阻滞细胞周期,诱导细胞分化和上调PPARγ蛋白及PPARγmRNA的核内表达,ATRA和RSG联合较单药作用效果更强.
목적 연구PPARγ격동제라격렬동(RSG)여전반식유갑산(ATRA)대인위암SGC7901세포주생장화조망적영향급기궤제적연구.방법 체외배양SGC7901세포,실험분위공백대조조、10μmol/L ATRA조、12.5 μmol/L RSG、25 μmol/L RSG조,10 μmol/L ATRA화25 μmol/L RSG연합조.MTT법검측세포생장억제솔,류식세포의측정세포주기,HE염색검측세포형태,면역세포화학검측PPARγ단백,RT-PCR검측PPARγmRNA.결과 10 μmol/L ATRA、12.5 mmol/L RSG、25 mmol/L RSG급량약연합시개가억제SGC7901세포적증식,차존재농도급시간의뢰,량약연합작용72 h시,생장억제솔위(29.73±0.69)%.ATRA、RSG개가사세포주기G0/G1기연장,S기하강,량약연합작용시,S%위(12.87±0.35)%,세포형태향정상방향전화,세포적PPARγ단백핵내표체급PPARγmRNA표체상조,량약연합후작용진일보가강,PPARγ/GAPDH적농도비치고체0.646.결론 ATRA、RSG균가억제SGC7901세포증식,조체세포주기,유도세포분화화상조PPARγ단백급PPARγmRNA적핵내표체,ATRA화RSG연합교단약작용효과경강.
Objective To investigate the influence of PPARγ excitomotor RSG and ATRA on gastric cancer SGC7901 cell line proliferation in vitro and its potential mechanism study.Methods Human gastric cancer SGC7901 cell line was cultured in vitro.Experiment samples were divided to blank group,10μmol/L ATRA group, 12.5μmol/L RSG group, 25μmol/L RSG group, 10μmol/L ATRA + 25μmol/L RSG group.Proliferation inhibitory effect was determined by MTI assay.Flow cytometry was used to detect cell cycle, H.E stain was used to observed micrography alteration.Expression of PPARγ protein in gastric cancer cells were measured by immunohistochemistry.PPARγ mRNA in gastric cancer cells were measured by RT-PCR.Results ATAR at concentration 10μmol/L, RSG at 12.5 μmol/L and RSG at 25 μmol/L could inhibit the proliferation of SGC7901 cells in a dose-and time-dependent, and when both agents were combined for 72h, growth inhibition ratio was (29.73 ± 0.69) %.Flow cytometry analysis revealed a cell cycle arrest at G1 and S phase, and when both agents combined, S% was (12.87 ± 0.35 )%, cell micrography tended to be normal when both agents combined.Up-regulation of PPARγ protein and PPARγ mRNA expressions were also observed, those effects were enhanced when both agents combined, and grey scale ratio was 0.646.Conclusion The ATRA and RSG could significantly induced growth inhibition of human gastric cancer SGC7901 cell, which may be associated with cell cycle arrest and inducing differentiation, activation of PPARγ protein and PPARγ mRNA expression.Synergistic effect could be caused by the combined use of the two agents.