Water-soluble chitosan inhibits the production of pro-inflammatory cytokine in human astrocytoma cells activated by amyloid beta peptide and interleukin-1beta

Neurosci Lett. 2002 Mar 15;321(1-2):105-9. doi: 10.1016/s0304-3940(02)00066-6.

Abstract

A chronic inflammatory response associated with beta-amyloid (Abeta) and interleukin-1beta (IL-1beta) is responsible for the pathology of Alzheimer's disease (AD). Astrocytes are predominant neuroglial cells of the central nervous system and are actively involved in cytokine-mediated events in AD. To investigate the biological effect of water-soluble chitosan (WSC), we examined cytotoxicity, production of pro-inflammatory cytokines and inducible nitric-oxide synthase (iNOS) on human astrocytoma cell line CCF-STTG1 stimulated with IL-1beta and Abeta fragment 25-35 (Abeta[25-35]). In 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazoliumbromide colorimetric assay, WSC by itself had no effect on cell viability on human astrocytoma cells. The effects of WSC on tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were evaluated with enzyme-linked immunosorbent assay and Western blotting. The production of TNF-alpha and IL-6 was induced by IL-1beta and Abeta[25-35] and synergistically amplified by the co-stimulation of IL-1beta and Abeta[25-35]. The secretion and expression of pro-inflammatory cytokines, TNF-alpha and IL-6, was significantly inhibited by pretreatment with WSC in human astrocytoma cells. The expression of iNOS was induced by IL-1beta and Abeta[25-35] and was partially inhibited by treatment with WSC. We demonstrate the regulatory effects of WSC in human astrocytes for the first time and suggest the anti-inflammatory effect of WSC may reduce and delay AD pathologic events.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / physiopathology
  • Amyloid beta-Peptides / antagonists & inhibitors*
  • Amyloid beta-Peptides / metabolism
  • Astrocytes / drug effects*
  • Astrocytes / metabolism
  • Astrocytoma
  • Brain / drug effects*
  • Brain / metabolism
  • Brain / physiopathology
  • Cell Survival / drug effects
  • Cell Survival / physiology
  • Chitin / analogs & derivatives
  • Chitin / pharmacology*
  • Chitosan
  • Cytokines / antagonists & inhibitors*
  • Cytokines / metabolism
  • Encephalitis / drug therapy*
  • Encephalitis / metabolism
  • Encephalitis / physiopathology
  • Humans
  • Interleukin-1 / antagonists & inhibitors*
  • Interleukin-1 / metabolism
  • Interleukin-6 / antagonists & inhibitors
  • Interleukin-6 / metabolism
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Amyloid beta-Peptides
  • Cytokines
  • Interleukin-1
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Chitin
  • Chitosan