Ginsenosides Inhibit HMGB1-induced Inflammatory Responses in HUVECs and in Murine Polymicrobial Sepsis

Title
Ginsenosides Inhibit HMGB1-induced Inflammatory Responses in HUVECs and in Murine Polymicrobial Sepsis
Author(s)
정태천이원화[이원화]구세광[구세광]이상규[이상규]배종섭[배종섭]
Keywords
VEIN ENDOTHELIAL-CELLS; GROUP BOX-1 PROTEIN; ADHESION MOLECULE EXPRESSION; GLYCATION END-PRODUCTS; TOLL-LIKE RECEPTORS; KAPPA-B ACTIVATION; PROINFLAMMATORY CYTOKINE; BARRIER DYSFUNCTION; DEPENDENT MECHANISM; THERAPEUTIC TARGET
Issue Date
201410
Publisher
KOREAN CHEMICAL SOC
Citation
BULLETIN OF THE KOREAN CHEMICAL SOCIETY, v.35, no.10, pp.2955 - 2962
Abstract
Asian ginseng is used as a treatment for cardiovascular diseases, ischemia, and cancers. High mobility group box 1 (HMGB1) protein acts as a late mediator of severe vascular inflammatory conditions. However, the effect of ginsenosides from Asian ginseng on HMGB1-induced inflammatory responses has not been studied. We addressed this question by monitoring the effects of ginsenoside treatment on lipopolysaccharide (LPS) and cecal ligation and puncture (CLP)-mediated release of HMGB1, and HIVIGB1-mediated regulation of proinflammatory responses. Ginsenoside treatment suppressed LPS-mediated release of HMGB1 and HMGB1-mediated cytoskeletal rearrangements. Ginsenosides also inhibited HMGB1-mediated inflammatory responses. In addition, ginsenosides inhibited the production of tumor necrosis factor-a (INF-alpha) and activation of protein kinase B (Akt), nuclear factor-kappa B (NF-kappa B), and extracellular-regulated kinases (ERK) 1/2 by HMGB1. Ginsenosides also decreased CLP-induced release of HMGB1, production of interleukin (M) 1 beta/6, and mortality. These results suggested that ginsenosides may be potential therapeutic agents for treatment of vascular inflammatory diseases through inhibition of the HMGB1 signaling pathway.
URI
http://hdl.handle.net/YU.REPOSITORY/30654http://dx.doi.org/10.5012/bkcs.2014.35.10.2955
ISSN
0253-2964
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약학대학 > 약학부 > Articles
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