MAPK信号通路在PM2.5致JurkatT细胞细胞因子改变中的调控作用  

Regulatory role of MAPK signaling pathway in the change of cytokines of Jurkat T cells induced by PM2.5

作　　者：张志红[1] 赵莹[1] 童国强[1] 刘杰静[1] 徐建军[1] 邱勇[1] 

机构地区：[1]山西医科大学公共卫生学院环境卫生学教研室,山西太原030001

出　　处：《现代预防医学》2014年第9期1562-1565,共4页Modern Preventive Medicine

基　　金：国家自然基金(81072261;30700655);山西省青年科技研究基金(2008021053);2009年山西省高校优秀青年学术带头人支持项目(晋教科2009-6号)

摘　　要：目的探讨MAPK信号通路对交通相关PM2.5引起JurkatT细胞细胞因子变化的调控作用。方法应用Western-blot方法测定了交通相关PM2.5刺激JurkatT细胞不同时间的磷酸化JNK、P38MAPK和激活蛋白-1(AP-1)蛋白表达,ELISA方法测定了细胞上清中肿瘤坏死因子-α(TNF-α)和白介素-1β(IL-1β)含量。结果 320μg/ml PM2.5刺激Jurkat T细胞24 h后,p-JNK/β-actin灰度比值显著高于生理盐水组,差异有统计学意义,P<0.05。80μg/ml、320μg/ml PM2.5组p-p38MAPK/β-actin灰度比值均高于生理盐水组,差异均有统计学意义,P<0.05。PM2.5染毒组分别加p-JNK拮抗剂SP600125和p-p38MAPK拮抗剂SB203580后,p-JNK/β-actin和p-p38MAPK/β-actin灰度比值均比正常染毒明显降低,以320μg/ml PM2.5剂量组显著。80μg/mlPM2.5刺激细胞6 h和24 h后,AP-1/β-actin蛋白灰度比值、细胞上清IL-1β含量均比生理盐水组增高,差异有统计学意义(P<0.05),80μg/ml PM2.5刺激细胞3 h、6 h和24 h后,细胞上清TNF-α逐渐增高,有明显的时间效应趋势,且与生理盐水组差异有统计学意义(P<0.05)。结论交通相关PM2.5可引起Jurkat T细胞炎症细胞因子TNF-α、IL-1β分泌增高,P38MAPK和JNK可通过AP-1调控TNF-α、IL-1β的释放。Objective To explore the regulatory role of MAPK signaling pathway in the change of cytokines of Jurkat T ceils induced by traffic-related PM2.5. Methods Expressions of the phosphorylation of JNK, P38MAPK and AP-1 protein in Jurkat T cells stimulated by traffic related PM2.5 for different time were determined by Western-blot method, and the levels of TNF- ct and IL-1 [3 in cells supernatant were detected by ELISA method. Results After 320 p~ g/ml of PM2.5 stimulated Jurkat T cells for 24h, p-JNK/[3 -actin gray level ratio was significantly higher than that in the normal saline group, and the difference was statistically significant. P-p38MAPK/[3 -actin intensity ratios in 80 p~ g/ml and 320 p^g/ml of PM2.5 groups were higher than those in the saline group, the difference was statistically significant （P〈0.05）. All exposed groups respectively with the p-JNK antagonist SP600125 or p-p38MAPK antagonist SB2035 80, p-JNK/[3 -aetin and p-p3gMAPK/β -actin gray ratio reduced than normal exposure groups, especially at 320 μg/ml of PM2.5 group. After 80 μg/ml of PM2.5 stimulated cells for 6h and 24h, AP-1/β -actin protein gray ratio, IL-1 β levels of cell supernatant were higher than normal saline group, the difference was significant （P〈0.05）. After 80 p^g/ml of PM2.5 stimulated cell for 3h, 6h and 24h, TNF- ct levels of cell supernatant increased gradually, had obvious time effect trend, and there was a significant difference in the normal saline group （P〈0.05）. Conchlslon Traffic-related PM2.5 can cause Jurkat T cells to release more inflammation cytokines TNF- α and IL-1 β, p38MAPK and JNK regulate the release of TNF- α and IL-1 β through AP-1.

关 键 词：PM2.5 交通污染 MAPK 细胞因子 激活蛋白-1 

分 类 号：R122[医药卫生—环境卫生学]