期刊
CHEMICO-BIOLOGICAL INTERACTIONS
卷 182, 期 1, 页码 29-36出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.cbi.2009.07.016
关键词
Apigenin; Fibroblast-like synoviocytes; Rheumatoid arthiritis; Reactive oxygen species; Mitogen-activated protein kinases; Apoptosis
资金
- Korea Science & Engineering Foundation [R01-2006-000-11359-0]
- [KRF-2006-005-J03401]
- National Research Foundation of Korea [R01-2006-000-11359-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Fibroblast-like synovial cells play a crucial role in the pathophysiology of rheumatoid arthritis (RA), as these cells are involved in inflammation and joint destruction. Apigenin, a dietary plant-flavonoid. is known to have many functions in animal cells including anti-proliferative and anticancer activities, but its role in human rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs) has not been reported. In this study, we investigated the roles of apigenin in RA-FLSs. The survival rate decreased, and apoptotic cell death was induced by apigenin treatment in PA-FLSs. Apigenin treatment resulted in activation of the. mitogen-activated protein kinase (MAPK) ERK1/2, and pretreatment with an ERK inhibitor PD98059 dramatically reduced apigenin-induced apoptosis. We found that apigenin-mediated production of a large amount of intracellular reactive oxygen species (ROS) caused activation of ERK1/2 and apoptosis: treatment with the antioxidant Tiron strongly inhibited the apigenin-induced generation of ROS, phosphorylation of ERK1112, and apoptotic cell death. Apigenin-induced apoptotic cell death was mediated through activation of the effectors caspase-3 and caspase-7, and was blocked by pretreatment with Z-VAD-FMK (a pan-caspase inhibitor). These results showed that apigenin-induced ROS and oxidative stress-activated ERK1/2 caused apoptotic cell death in apigenin-treated RA-FLSs. (C) 2009 Elsevier Ireland Ltd All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据