CAJ | 학술논문

目的探讨过氧化物酶体增殖物激活受体y(PPART)激动剂罗格列酮(msiglitazone,RGZ)对白血病K562细胞的诱导凋亡作用及其作用机制.方法以不M浓度的RGZ(20～80umol/L)作用于体外培养的K562细胞0,24、48、72 h,应用噻唑蓝法检测细胞生长抑制率,用膜联蛋白v.碘化丙啶双染法检测细胞凋亡,并对细胞凋亡前后1'53蛋白的表达水平及Caspse.3活性进行榆测.结果 40~moVL以上的RGZ可显著抑制细胞生长及诱导细胞发生凋亡,呈现出明显的量效与时效关系,在细胞凋亡的同时,P53蛋白的表达水平及Caspse-3活性均明显升高.结论 40umol/L以上的RGZ能显著抑制K562细胞的生长并诱导细胞发生凋亡,升高半胱天冬蛋白酶(Caspse)-3活性,上涮促凋亡蛋白P53的表达水平是RGZ诱导K562细胞发生凋亡的重要作用机制之一.
목적 탐토과양화물매체증식물격활수체y(PPART)격동제라격렬동(msiglitazone,RGZ)대백혈병K562세포적유도조망작용급기작용궤제.방법 이불M농도적RGZ(20～80umol/L)작용우체외배양적K562세포0,24、48、72 h,응용새서람법검측세포생장억제솔,용막련단백v.전화병정쌍염법검측세포조망,병대세포조망전후1'53단백적표체수평급Caspse.3활성진행유측.결과 40~moVL이상적RGZ가현저억제세포생장급유도세포발생조망,정현출명현적량효여시효관계,재세포조망적동시,P53단백적표체수평급Caspse-3활성균명현승고.결론 40umol/L이상적RGZ능현저억제K562세포적생장병유도세포발생조망,승고반광천동단백매(Caspse)-3활성,상쇄촉조망단백P53적표체수평시RGZ유도K562세포발생조망적중요작용궤제지일.
Objective To investigate the apoptosis inducing effect of peroxisome proliferator-activated receptor r(PPARr)agomst on leukemic K562 cells and its mechanisms of action.Methods K562 cells in culture medium in vitro were given different concentrations of PPARragonist rosiglitazone(RGZ)(20-80 umol/L)for O,24,48 and 72h The inhibitory rate of the cells were measured by MTT assay,cell apoptosis was detected by Annexin V/PI staining,and the expression of P53 protein as well as the activity of caspase-3 were also detected.Results RGZ(over 40umoL/L)could inhibit the growth of K562 cells and cause apopto-sis remarkably,the suppression Was both in time-and dose-dependent manner.The expression of P53 pmtein was upregulated and the activity of caspase-3 Was increased concomitantly after the cells werle treated by RGZ.Conclusion PPARr agonist RGZ(over 40 umol/L)can induce apoptosis on K562 cells signifieantly,upregu-lation the expression of P53 protein as well as increasing caspase-3 activity may be one of its most important mechamisms.