PPAR-γ配体对T淋巴瘤细胞NO生成诱导时间效应的研究  

Study on the time effect of NO production induced by PPAR-γ ligand in Jurkat cells

作　　者：金呈强[1] 刘仿[1] 王文涓[1] 肖红[2] 周细玉[1] 

机构地区：[1]广东医学院微生物与免疫学教研室,广东湛江524023 [2]广东医学院第一附属医院儿科,广东湛江524000

出　　处：《临床和实验医学杂志》2009年第3期1-3,共3页Journal of Clinical and Experimental Medicine

基　　金：广东省自然科学基金(No:06028959);东莞市科技计划项目(No:2008108101033)

摘　　要：目的探讨在人类Jurkat系T肿瘤细胞内,过氧化物酶体增生物激活受体γ(PPAR-γ)对一氧化氮(NO)生成的影响及意义。方法Jurkat系T淋巴肿瘤细胞分成对照组和试验组。试验组用相同浓度(20μmol/L)的PPAR-γ激活剂噻唑烷二酮(TZD)类药物罗格列酮刺激Jurkat系T肿瘤细胞(对照组不加药物),用药6h、12h、18h、24h和30h后用硝酸还原酶法检测NO含量,反转录聚合酶链(RT-PCR)法检测T肿瘤细胞PPAR-γmRNA表达情况。结果PPAR-γ的含量随着用药时间的延长而升高,用药后NO在第6h、12h、18h、24h和30h的含量均显著高于用药前NO的含量(P<0.05),NO表达量与PPAR-γ的表达呈正相关(r=0.87,P<0.05)。结论在Jurkat系T肿瘤细胞内,PPAR-γ活化剂能够以时间依赖的形式增加NO生成,PPAR-γ可能通过NO途径来发挥相应的生理功能。Objective Peroxisome proliferator - activated receptor （ PPAR - γ） has a comprehensive anti - cancer activity, whether PPAR - 3, anti - tumor effect is mediated by nitric oxide （NO） pathway is not clear at present. This study aimed to investigate the influence and significance of PPAR - γ on NO production in Jurkat human T lymphoma cell line. Methods Jurkat cells Were stimulated with 20μmol / L of rosiglitazone （PPAR -γ activator） in experimental group. Rosiglitazone was not added in the cells in control group. NO content was detected by using nitrate reductase and PPAR - γ mRNA expression was detected by RT - PCR 6 h, 12 h , 18 h, 24 h and 30 h after treatment. Results The expressions of PPAR - γmRNA were increased gradually with time after medication. NO contents were signitlcantly higher than those in the control group 6 h, 12 h, 18 h, 24 h and 30 h after treatment and the expressions of PPAR -γ and the contents of NO showed positive correlation （ r =0.87, P 〈 0.05 ）. Conclusion PPAR -γ activator stimulates NO production in a time - dependent mode in Jurkat cells. It is suggested that PPAR -γ might adjust target factors by NO pathway in Jurkat cells.

关 键 词：一氧化氮 一氧化氮合酶 T肿瘤细胞 PPAR-Γ 

分 类 号：R733.1[医药卫生—肿瘤]