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Proinflammatory activation of macrophages by bisphenol A-glycidyl-methacrylate involved NFκB activation via PI3K/Akt

Yu-Hsiang Kuan1, Fu-Mei Huang, Yi-Ching Li

  • 1Department of Pharmacology, Chung Shan Medical University, Taichung, Taiwan.

Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association
|September 4, 2012
PubMed
Abstract

Insights

Bisphenol A-glycidyl-methacrylate (BisGMA), a dental resin, activates macrophages, inducing inflammatory mediators like nitric oxide and cytokines. This suggests BisGMA may trigger inflammation through NF-κB and Akt pathways.

Area of Science:

  • Biomaterials Science
  • Immunology
  • Cell Biology

Background:

  • Bisphenol A-glycidyl-methacrylate (BisGMA) is a common dental composite resin.
  • BisGMA may cause inflammatory effects on adjacent tissues.
  • The mechanisms of BisGMA-induced macrophage activation are not well understood.

Purpose of the Study:

  • To investigate the effects of BisGMA on proinflammatory mediator generation in murine macrophage RAW264.7 cells.
  • To elucidate the signaling pathways involved in BisGMA-induced macrophage activation.

Main Methods:

  • Murine macrophage RAW264.7 cells were treated with BisGMA.
  • Proinflammatory mediators (IL-1β, IL-6, nitric oxide, ROS) were quantified.
  • Expression of key signaling proteins (iNOS, p-p65, IκB, p-Akt) was analyzed via Western blotting.

Main Results:

  • BisGMA dose-dependently increased IL-1β, IL-6, nitric oxide, and iNOS expression.
  • BisGMA dose-dependently enhanced intracellular and extracellular reactive oxygen species (ROS) generation.
  • BisGMA time- and dose-dependently increased p65 phosphorylation, IκB degradation, and Akt phosphorylation.

Conclusions:

  • BisGMA induces nitric oxide, ROS, and inflammatory cytokines in macrophages.
  • BisGMA activates macrophages potentially through NF-κB and Akt signaling pathways.

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