熊果酸诱导Jurkat细胞凋亡及其作用机制的研究  

Inducing Effects of Ursolic Acid on Jurkat Cell Apoptosis and Its Mechanisms

作　　者：贾文文[1] 苗苗[1] 李佳[1] 吴斌[1] 刘卓刚[1] 

机构地区：[1]中国医科大学附属盛京医院血液病治疗中心,辽宁沈阳110022

出　　处：《中国实验血液学杂志》2014年第2期310-314,共5页Journal of Experimental Hematology

基　　金：辽宁省科技厅科学技术计划项目(2010225032)

摘　　要：本研究观察熊果酸(ursolic acid,UA)对人T细胞白血病/淋巴瘤细胞(Jurkat)凋亡的影响及其初步作用机制。用不同浓度UA在不同时间处理Jurkat细胞,采用细胞毒性试验(CCK8法)检测细胞增殖情况;应用荧光显微镜及流式细胞术检测细胞凋亡;实时定量PCR检测PTEN mRNA的表达水平。结果表明:UA在10-80μmol/L的浓度范围内能抑制Jurkat细胞的生长,并呈现剂量-时间依赖性;UA 40、80μmol/L处理Jurkat细胞24、48 h后,出现凋亡细胞,并可见其细胞核呈波纹状或折缝样,荧光染色增强。UA诱导Jurkat细胞凋亡的作用呈浓度依赖性,与同时间对照组比较差异有统计学差异(P<0.05);与同时间对照组相比,UA能够增加PTEN mRNA的表达。结论:UA可以上调PTEN mRNA的表达,并可能通过此机制诱导Jurkat细胞凋亡。The study was aimed to investigate the inducing effect of ursolic acid （UA） on the apoptosis of human T- cell leukemia/lymphoma （Jurkat）, and whether the regulation of PTEN involved in the effect of UA on Jurkat cells. The Jurkat cells were treated with different concentrations of UA for different time. The cell proliferation was analyzed with cytotoxicity test （CCK8 method）. Cell apoptosis was detected by fluorescence microscopy and flow cytometry. The expression of PTEN mRNA was detected by real-time quantitative PCR. The results indicated that UA could significantly inhibite the viability of Jurkat cells treated with 10 - 80 μ mol/L and in dose- and time-dependent manner. UA could induce Jurkat cell apoptosis in a dose-dependent manner, which was statistical different from the control at the same time （ P 〈 0.05 ）. PTEN mRNA expression was up-regulated by UA, which was statistical different from the control （ P 〈 0.05 ）. It is concluded that UA may induce Jurkat cell apoptosis by up-regulating the PTEN mRNA expression.

关 键 词：熊果酸 JURKAT细胞 细胞凋亡 PTEN 

分 类 号：R733.7[医药卫生—肿瘤] R979.1[医药卫生—临床医学]