Polysaccharides from Bupleurum chinense impact the recruitment and migration of neutrophils by blocking fMLP chemoattractant receptor-mediated functions

Carbohydr Polym. 2013 Feb 15;92(2):1071-7. doi: 10.1016/j.carbpol.2012.10.059. Epub 2012 Oct 30.

Abstract

Although neutrophils play important roles in host defense, sometimes they contribute to inflammation-related tissue injuries. Thus, restriction of their recruitment to the inflammatory sites is a promising strategy in the amelioration of inflammatory disease. The previous studies reported the anti-inflammatory effects of Bupleurum chinense, but the active ingredients and possible mechanism are still unclear. Here, we isolated water-soluble polysaccharides (BCPs) from B. chinense, to evaluate its anti-inflammatory effects and possible mechanism. The present results showed that BCPs significantly impaired the in vivo neutrophil infiltration, as well as the migration capacity of dHL-60 cells in vitro. In addition, BCPs inhibits chemoattractant fMLP-induced activation and clustering of β2 integrin. BCPs impacted fMLP-induced actin polymerization and the activation of cytoskeleton regulatory molecules, Vav1 and Rac1. Together, BCPs significantly impacted recruitment and migration of neutrophils by blocking chemoattractant receptor-mediated functions, and it possesses a potential as novel anti-inflammatory drug.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / chemistry
  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Bupleurum / chemistry*
  • CD18 Antigens / metabolism
  • HL-60 Cells
  • Humans
  • Male
  • Mice
  • Mice, Inbred BALB C
  • N-Formylmethionine Leucyl-Phenylalanine / metabolism*
  • N-Formylmethionine Leucyl-Phenylalanine / pharmacology
  • Neutrophil Infiltration / drug effects*
  • Neutrophils / cytology
  • Neutrophils / drug effects
  • Neutrophils / immunology
  • Polysaccharides / pharmacology*
  • Protein Multimerization / drug effects
  • Protein Structure, Quaternary
  • Proto-Oncogene Proteins c-vav / metabolism
  • Receptors, Formyl Peptide / antagonists & inhibitors*
  • Receptors, Formyl Peptide / metabolism*
  • Signal Transduction / drug effects
  • Signal Transduction / immunology
  • rac1 GTP-Binding Protein / metabolism

Substances

  • Actins
  • Anti-Inflammatory Agents
  • CD18 Antigens
  • Polysaccharides
  • Proto-Oncogene Proteins c-vav
  • Receptors, Formyl Peptide
  • VAV1 protein, human
  • N-Formylmethionine Leucyl-Phenylalanine
  • rac1 GTP-Binding Protein