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KMID : 0043320130360091160
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Archives of Pharmacal Research
2013 Volume.36 No. 9 p.1160 ~ p.1165
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Emodin-6-O-β-d-glucoside down-regulates endothelial protein C receptor shedding
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Lee Won-Hwa
Ku Sae-Kwang
Bae Jong-Sup
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Abstract
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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-α 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-β-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.
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KEYWORD
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Emodin-6-O-β-d-glucoside, EPCR, Shedding, PMA
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