Modified Si-Miao-San extract inhibits the release of inflammatory mediators from lipopolysaccharide-stimulated mouse macrophages

J Ethnopharmacol. 2010 May 4;129(1):5-9. doi: 10.1016/j.jep.2010.02.002. Epub 2010 Feb 20.

Abstract

Ethnopharmacological relevance: Modified Si-Miao-San (mSMS) is a prescription modified from Si-Miao-San which is an ancient Chinese prescription used to treat various ailments.

Aim of the study: Modified Si-Miao-San (mSMS) has been used for the treatment of infectious and inflammatory disorders in the clinic. This study was aimed to investigate its anti-inflammatory activity and underlying mechanism at cellular and molecular levels.

Materials and methods: We stimulated RAW264.7 cells with Lipopolysaccharide (LPS) and observed effects of mSMS on the release of inflammatory mediators such as: tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), NO, and relative gene expressions. Meanwhile, we also investigated the modulation of mSMS in inflammatory signal transduction mediated through extracellular signal-regulated protein kinase (ERK) and nuclear factor-kappaB (NF-kappaB) pathway.

Results: Our findings demonstrated that mSMS significantly inhibited the excessive production of NO, TNF-alpha and IL-6 and the over expression of relative genes in LPS-stimulated macrophages. In addition, mSMS suppressed LPS-induced ERK1/2-phosphorylation and inhibited the activation of NF-kappaB by attenuation of I kappaB-alpha degradation.

Conclusions: Our results suggest that the anti-inflammatory properties of mSMS might result from the inhibition of inflammatory mediators, such as NO, TNF-alpha and IL-6, via suppression of ERK and NF-kappaB dependent pathways.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Drugs, Chinese Herbal / pharmacology*
  • Extracellular Signal-Regulated MAP Kinases / metabolism*
  • Gene Expression
  • I-kappa B Proteins / metabolism
  • Inflammation / drug therapy
  • Inflammation Mediators / metabolism*
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism
  • Lipopolysaccharides
  • Macrophages / drug effects*
  • Magnoliopsida
  • Mice
  • NF-kappa B / metabolism*
  • Nitric Oxide / genetics
  • Nitric Oxide / metabolism
  • Phosphorylation
  • Signal Transduction / drug effects
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents
  • Drugs, Chinese Herbal
  • I-kappa B Proteins
  • Inflammation Mediators
  • Interleukin-6
  • Lipopolysaccharides
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • Extracellular Signal-Regulated MAP Kinases