| In vitro: |
| Arch Pharm Res . 2013 Sep;36(9):1160-5. | | Emodin-6-O-β-D-glucoside down-regulates endothelial protein C receptor shedding[Pubmed: 23588681] | | 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. | | Inflammation . 2014 Apr;37(2):306-13. | | Emodin-6-O-β-D--glucoside inhibits high-glucose-induced vascular inflammation[Pubmed: 24114447] | | Emodin-6-O-β-D-glucoside (EG), a new active compound from Reynoutria japonica, has recently been shown to exert potent anti-inflammatory and barrier protective effects in human umbilical vein endothelial cells (HUVECs) and in mice. Vascular inflammatory process has been suggested to play a key role in initiation and progression of atherosclerosis, a major complication of diabetes mellitus. Thus, we attempted to determine whether EG can suppress the vascular inflammatory process induced by high glucose (HG) in HUVECs and mice. Data showed that HG induced markedly increased vascular permeability, monocyte adhesion, expressions of CAMs, formation of ROS, and activation of NF-κB. Remarkably, all of the above-mentioned vascular inflammatory effects of HG were attenuated by pretreatment with EG. Vascular inflammatory responses induced by HG are critical events underlying development of various diabetic complications; therefore, our results suggest that EG may have significant therapeutic benefits against diabetic complications and atherosclerosis. |
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| In vivo: |
| Food Chem Toxicol . 2013 Feb;52:97-104. | | Emodin-6-O-β-D-glucoside inhibits HMGB1-induced inflammatory responses in vitro and in vivo[Pubmed: 23146691] | | High mobility group box 1 (HMGB1) protein acts as a potent proinflammatory cytokine and is involved in the pathogenesis of several vascular diseases, such as, systemic vasculitis and sepsis. Emodin-6-O-β-D-glucoside (EG) is a new active compound from Reynoutria japonica, and its biologic activities have not been previously investigated. In this study, we first investigated the antiinflammatory activities of EG on HMGB1-mediated proinflammatory responses in human umbilical vein endothelial cells (HUVECs) and in a murine cecal ligation and puncture (CLP)-model of sepsis in mice. EG was found to suppress the release of HMGB1, the production of tumor necrosis factor (TNF)-α, and the activation of nuclear factor-κB (NF-κB) by HMGB1 in HUVECs, and to inhibit HMGB1-mediated hyperpermeability and leukocyte migration in mice. In the CLP model, HMGB1 was highly released, but this release was prevented by EG. Furthermore, EG also increased the survival times of CLP administered mice. Collectively, this study shows EG can protect barrier integrity and inhibit HMGB1-mediated inflammatory responses, which suggests a potential use as a therapy for sepsis or septic shock. |
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Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.IF=36.216(2019)
Cell Metab. 2020 Mar 3;31(3):534-548.e5. doi: 10.1016/j.cmet.2020.01.002.IF=22.415(2019)
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.IF=14.548(2019)
ACS Nano. 2018 Apr 24;12(4): 3385-3396. doi: 10.1021/acsnano.7b08969.IF=13.903(2019)
Nature Plants. 2016 Dec 22;3: 16206. doi: 10.1038/nplants.2016.205.IF=13.297(2019)
Sci Adv. 2018 Oct 24;4(10): eaat6994. doi: 10.1126/sciadv.aat6994.IF=12.804(2019)
