Please use this identifier to cite or link to this item:
|標題:||KINSENOSIDE ISOLATED FROM ANOECTOCHILUS FORMOSANUS SUPPRESSES LPS-STIMULATED INFLAMMATORY REACTIONS IN MACROPHAGES AND ENDOTOXIN SHOCK IN MICE||作者:||Hsiao, H.B.
|關鍵字:||Cytokine;inflammation;kinsenoside;LPS;nf-kappa-b;kupffer cells;nitric-oxide;il-10;involvement;expression;sepsis;alpha;mcp-1||Project:||Shock||期刊/報告no：:||Shock, Volume 35, Issue 2, Page(s) 184-190.||摘要:||
In the present study, we reported that kinsenoside, a major component of Anoectochilus formosanus, inhibited inflammatory reactions in mouse peritoneal lavage macrophages and protects mice from endotoxin shock. In LPS-stimulated mouse peritoneal lavage macrophages, kinsenoside inhibited the inflammatory mediators, such as nitric oxide, TNF-alpha, IL-1 beta, monocyte chemoattractant protein 1, and macrophage migration inhibitory factor production. Furthermore, kinsenoside decreased the formation of a nuclear factor kappa B-DNA complex and nuclear p65 and p50 protein levels. Kinsenoside inhibited nuclear factor kappa B translocation through both I kappa B alpha-dependent and -independent pathway. In contrast, it stimulated anti-inflammatory cytokine IL-10 generation and enhanced the mRNA expression of IL-10 and suppressor of cytokine signaling 3 in the same cells induced by LPS. In an animal model, both pretreatment and posttreatment of kinsenoside increased the survival rate of ICR mice challenged by LPS (80 mg/kg, i.p.). Pretreatment with kinsenoside decreased serum levels of TNF-alpha, IL-1 beta, IL-10, monocyte chemoattractant protein 1, and migration inhibitory factor at 1 h after sublethal dose of LPS (40 mg/kg, i. p.) in mice. In contrast, kinsenoside enhanced serum IL-10 level at 24 h after LPS injection in mice. In conclusion, kinsenoside inhibited the production of inflammatory mediators and enhanced anti-inflammatory cytokine generation. Therefore, kinsenoside can alleviate acute inflammatory hazards.
|Appears in Collections:||生命科學系所|
Show full item record
TAIR Related Article
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.