Forsythoside B Protects Against Experimental Sepsis by Modulating Inflammatory Factors
Article first published online: 6 DEC 2011
Copyright © 2011 John Wiley & Sons, Ltd.
Volume 26, Issue 7, pages 981–987, July 2012
How to Cite
Jiang, W.-L., Yong-Xu, Zhang, S.-P., Zhu, H.-B. and Jian-Hou (2012), Forsythoside B Protects Against Experimental Sepsis by Modulating Inflammatory Factors. Phytother. Res., 26: 981–987. doi: 10.1002/ptr.3668
- Issue published online: 5 JUL 2012
- Article first published online: 6 DEC 2011
- Manuscript Accepted: 1 SEP 2011
- Manuscript Revised: 30 AUG 2011
- Manuscript Received: 28 APR 2011
- Forsythoside B;
- septic shock;
- triggering receptor expressed on myeloid cells;
- caecal ligation and puncture
The present study investigated the effects of Forsythoside B on an experimental model of sepsis induced by caecal ligation and puncture (CLP) in rats and elucidated the potential mechanism in cultured RAW 264.7 cells. Results showed that Forsythoside B concentration-dependently down-regulated the levels of TNF-α, IL-6 and high-mobility group-box 1 protein (HMGB1) in lipopolysaccharide (LPS)-stimulated RAW264.7 cells, inhibited the IκB kinase (IKK) pathway and modulated nuclear factor (NF)- κB. Intravenous injection (i.v.) of Forsythoside B alone or plus Imipenem reduced serum levels of TNF-α, IL-6, HMGB1, triggering receptor expressed on myeloid cells (TREM-1) and endotoxin, while the serum level of IL-10 was up-regulated and myeloperoxidase (MPO) in lung, liver and small intestine was reduced. Meanwhile, i.v. of Forsythoside B alone or plus Imipenem reduced CLP-induced lethality in rats. These data indicated that the antisepsis effect of Forsythoside B is mediated by decreasing local and systemic levels of a wide spectrum of inflammatory mediators. Its antisepsis mechanism may be that Forsythoside B binds to LPS and reduces the biological activity of serum LPS, and inhibits NF-κB activition. Our studies enhance the case for the use of Forsythoside B in sepsis. Forsythoside B itself has promise as a therapy for the treatment of sepsis in humans. Copyright © 2011 John Wiley & Sons, Ltd.