PPARγ激动剂对白血病NB4细胞的诱导凋亡作用及其作用机制  

Mechanistic Study of Peroxisome Proliferator-Activated Receptor γ(PPARγ) Agonist Induced Apoptosis of NB4 Cells

作　　者：刘晓丽[1] 林东军[2] 肖若芝[2] 刘加军[2] 

机构地区：[1]上海交通大学附属新华医院血液科,上海200092 [2]中山大学附属第三医院血液科,广州510630

出　　处：《热带医学杂志》2009年第1期4-6,共3页Journal of Tropical Medicine

基　　金：国家自然科学基金(No.30570786);教育部新世纪优秀人才支持计划资助项目(No.NCET-06-0721)

摘　　要：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 apoptosis inducing effect of peroxisome proliferator-activated receptor （PPARγ） agonist on leukemic NB4 cells. Methods NB4 cells were incubated with different concentrations of PPAR＇y agonist rosiglitazone （RGZ） for 0, 24, 48 and 72 h. The growth of NB4 cells were measured by MTT assay. Aapoptosis was measured by Annexin V/PI staining method. The expression of P53 protein was determined by flowcytometry. Results RGZ was found to induce growth inhibition and apoptosis of NB4 cells in a time- and dosedependent manner. The expression of P53 protein was upregulated after the cells were treated with RGZ. Conclusion PPARγ agonist RGZ can significantly induce apoptosis on NB4 cells. The induction of apoptosis may be through the upregulation of the expression of P53 protein.

关 键 词：过氧化物酶体增殖物激活受体Γ NB4细胞 细胞凋亡 白血病 

分 类 号：R733.7[医药卫生—肿瘤]