期刊
ARCHIVES OF PHARMACAL RESEARCH
卷 36, 期 9, 页码 1160-1165出版社
PHARMACEUTICAL SOC KOREA
DOI: 10.1007/s12272-013-0114-6
关键词
Emodin-6-O-beta-D-glucoside; EPCR; Shedding; PMA
资金
- National Research Foundation of Korea (NRF)
- Korea government [MEST] [2012-0009400]
- Korean Health Technology R&D Project, Ministry of Health & Welfare, Republic of Korea [A111305]
- Korea Health Promotion Institute [A111305] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Endothelial protein C receptor (EPCR) plays an important role in the protein C anticoagulation pathway and in the cytoprotective pathway. Previously, EPCR can be shed from the cell surface, which is mediated by tumor necrosis factor-alpha converting enzyme (TACE). Soluble EPCR levels are increased in patients with systemic inflammatory diseases. Recently, we reported that a new active compound, emodin-6-O-beta-d-glucoside (EG) from Reynoutria japonica, has anti-inflammatory activities. However, little is known of the effects of EG on EPCR shedding. Here, we investigated this issue by monitoring the effects of EG on the phorbol-12-myristate 13-acetate (PMA) or the cecal ligation and puncture (CLP)-mediated EPCR shedding and its underlying mechanisms. Data showed that EG potently inhibited the PMA and CLP-induced EPCR shedding by suppressing TACE expression. Given these results, EG could be used as a candidate therapeutic for the treatment of vascular inflammatory diseases.
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