[Advanced oxidation protein products-induced tumor necrosis factor alpha secretion in monocytes via reactive oxygen species generation]

Di Yi Jun Yi Da Xue Xue Bao. 2005 May;25(5):493-7.
[Article in Chinese]

Abstract

Objective: To investigate the effect of advanced oxidation protein products (AOPP) on the secretion of tumor necrosis factor alpha eTNFalphae in monocytes and its possible mechanism.

Method: Human monocyte cell line THP-1 and peripheral blood monocytes were incubated with AOPP-bovine serum albumin(BSA) prepared by incubation of BSA with hypochlorous acid. TNFalpha in the supernatant of the culture medium of THP-1 cells was measured by enzyme-linked immunosorbent assay and the production of reactive oxygen species (ROS) evaluated by measuring the fluorescent product from the oxidation of an oxidant-sensitive 2,7-dichlorefluorescin using Wallac 1420 multilabel counter. The intracellular signal was observed by pre-treatment of the cells with antioxidant pyrrolidine dithiocarbamate, NADPH oxidase inhibitor apocynin or p38 phosphorylation inhibitor SB203580.

Results: AOPP-BSA induced TNF-alpha secretion and ROS production in monocytes. Pretreatment of the cells with pyrrolidine dithiocarbamate scavenged most of ROS and almost completely blocked TNF-alpha secretion induced by AOPP-BSA. Inhibition of NADPH oxidase by apocynin and p38 phosphorylation by SB203580 could both effectively block AOPP-BSA-induced TNF-alpha secretion.

Conclusion: AOPP-BSA induced TNF-alpha secretion in monocytes, and the intracellular signaling involves ROS produced by activated NADPH oxidase and subsequent p38 phosphorylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blood Proteins / chemistry
  • Blood Proteins / metabolism
  • Cells, Cultured
  • Humans
  • Monocytes / metabolism*
  • NADPH Oxidases / metabolism
  • Oxidation-Reduction
  • Oxidative Stress*
  • Reactive Oxygen Species / metabolism*
  • Tumor Necrosis Factor-alpha / metabolism*
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Blood Proteins
  • Reactive Oxygen Species
  • Tumor Necrosis Factor-alpha
  • NADPH Oxidases
  • p38 Mitogen-Activated Protein Kinases