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目的探讨过氧化物酶体增殖物激活受体γ(PPARγ)激动剂罗格列酮(rosiglitazone,RGZ)对白血病NB4细胞的诱导凋亡作用及其作用机制。方法以不同浓度的RGZ作用于体外培养的NB4细胞0、24、48及72h,应用MTT法检测细胞生长抑制率,用Annexin V/PI双染法检测细胞凋亡,并对细胞凋亡前后P53蛋白的表达水平进行检测。结果RGZ可显著抑制细胞的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蛋白的表达水平明显升高。结论PPARγ激动剂RGZ能显著抑制NB4细胞的生长并诱导细胞发生凋亡,升高促凋亡蛋白P53的表达水平可能是RGZ诱导NB4细胞发生凋亡的重要作用机制之一。
Objective To investigate the effect of peroxisome proliferator - activated receptor γ (PPARγ) agonist rosiglitazone (RGZ) on the apoptosis of leukemic NB4 cells and its mechanism. Methods Different concentrations of RGZ were applied to NB4 cells cultured in vitro for 0, 24, 48 and 72 h. Cell growth inhibition rate was detected by MTT assay. Apoptosis was detected by Annexin V / PI double staining. P53 Protein expression levels were tested. Results RGZ could significantly inhibit cell growth and induce cell apoptosis, showing a dose-effect-time-effect relationship. At the same time of apoptosis, P53 protein expression was significantly increased. Conclusion PPARγ agonist RGZ can significantly inhibit the growth of NB4 cells and induce the apoptosis of cells. Increasing the expression of pro-apoptotic protein P53 may be one of the important mechanisms of RGZ-induced NB4 cell apoptosis.