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目的:探讨过氧化物酶体增殖因子活化受体γ(PPARγ)配体罗格列酮(ROS)对人急性单核细胞白血病U937细胞生长抑制作用及其作用机制。方法:体外培养人急性单核细胞白血病U937细胞,应用不同浓度的罗格列酮处理人急性单核细胞白血病U937细胞,采用MTT比色法测定药物对细胞增殖的抑制作用;用流式细胞术、AnnexinⅤ/PI双染色法观察细胞凋亡率;并分析细胞周期改变;RT-PCR法分析PPARγmRNA表达。结果:ROS浓度>80μmol/L时,对U937细胞产生明显的增殖抑制作用,P<0.05;AnnexinⅤ/PI双染色法观察细胞凋亡率>50%,并将细胞周期阻滞在G1期,P<0.05;RT-PCR检测U937细胞中PPARγmRNA表达无明显变化。结论:ROS浓度>80μmol/L时,对U937细胞产生明显的增殖抑制作用及诱导凋亡作用,同时将细胞周期阻滞在G1期,但是PPARγmRNA表达无明显变化,推测可能与激活PPARγ表达无明显相关,可能存在另外的信号转导途径。
AIM: To investigate the inhibitory effect of peroxisome proliferator-activated receptor γ (PPARγ) ligand rosiglitazone (ROS) on human acute monocytic leukemia U937 cells and its mechanism. Methods: Human acute monocytic leukemia U937 cells were cultured in vitro. Rosiglitazone at different concentrations was used to treat human acute monocytic leukemia U937 cells. MTT assay was used to determine the inhibitory effect of drugs on cell proliferation. Flow cytometry , Annexin Ⅴ / PI double staining was used to observe the apoptosis rate. The changes of cell cycle were analyzed. The expression of PPARγ mRNA was analyzed by RT-PCR. Results: The proliferation of U937 cells was inhibited by ROS at a concentration of> 80μmol / L (P <0.05). The apoptotic rates of cells were observed by AnnexinⅤ / PI double staining. The cell cycle arrest was at G1 phase, P <0.05; No significant change of PPARγmRNA expression in U937 cells was detected by RT-PCR. CONCLUSION: ROS concentration> 80μmol / L can significantly inhibit the proliferation of U937 cells and induce apoptosis. At the same time, the cell cycle arrests in G1 phase but there is no obvious change in PPARγ mRNA expression, which may be related to the activation of PPARγ expression Related, there may be additional signal transduction pathways.