中国药理学通报2012，Vol.28Issue(9)：1303-1307,5.DOI:10.3969/j.issn.1001-1978.2012.09.027
DATS通过p38MAPK通路抑制LPS诱导的小鼠MH-S细胞TNF-α及IL-1β表达
Inhibition of LPS-induced TNF-α and IL-1β expression by DATS through p38 MAPK pathway in MH-S cell
摘要
Abstract
Aim To investigate the role of p38 mito-gen activated protein kinase ( MAPK ) in the signal transduction mechanisms of diallyl trisulfide ( DATS ) inhibiting the tumor necrosis factor ( TNF-α ) and in-terleukin-1β ( IL-1β ) expression induced by lipopo- lysaccharide ( LPS ) in mouse alveolar macrophages cell line MH-S. Methods MH-S cells were cultured in vitro, and treated with DATS in the presence or absence of LPS for different time. The expression of phospho- p 3 8 and p38 were assayed by Western blot.ls MH-S cells were incubated with specific p38 inhibitor SB203580 in the presence or absence of LPS. The expression of TNF-α mRNA and IL-1β mRNA were detected with reverse transcription-PCR ( RT-PCR ). The expression of phospho-IκB and IκB were assayed by Western blot. Results The expression of the phospho-p38 expression in MH-S increased markedly under the stimulation of LPS in a time-dependent manner. Pre-treatment with DATS( 0. 1, 0. 5, 2. 5, 5. 0 mg · L-1 ) for 30min prior to LPS activation resulted in an obvious reduction of phospho-p38 expression in a dose-dependent manner. DATS alone did not influence the phos- pho-p38 expression. SB203580 dose-dependently inhibited LPS-induced TNF-a mRNA, IL-1β mRNA expression and phospho-IκB expression. Conclusions DATS downregulates TNF-α and IL-1β mRNA expression in LPS-stimulated MH-S by inhibiting the p38MAPK pathway and the subsequent phosphorylation of IκB and NF-κB activation.关键词
二烯丙基三硫/脂多糖/肺泡巨噬细胞/p38丝裂原活化蛋白激酶/核因子-κB/肿瘤坏死因子α/白细胞介素1βKey words
diallyl trisulfide( DATS )/ lipopolysaccha-ride( LPS )/ alveolar macrophages/ p38 mitogen activated protein kinase( p38 MAPK )/ nuclear factor-κB ( NF-κB )/ tumor necrosis factor-α( TNF-α )/ interleu-kinlp(lL-1β)分类
医药卫生引用本文复制引用
朱桂军,孟志强,刘丽霞,武新慧,王澜涛,陈玉红,胡振杰..DATS通过p38MAPK通路抑制LPS诱导的小鼠MH-S细胞TNF-α及IL-1β表达[J].中国药理学通报,2012,28(9):1303-1307,5.基金项目
河北省科技攻关资助项目(No 05276101D-65) （No 05276101D-65）
