Apigenin inhibits release of inflammatory mediators by blocking the NF-κB activation pathways in the HMC-1 cells

Immunopharmacol Immunotoxicol. 2011 Sep;33(3):473-9. doi: 10.3109/08923973.2010.538851. Epub 2010 Dec 13.

Abstract

Apigenin is a plant flavonoid and a pharmacologically active agent that has been isolated from several plant species. However, the molecular mechanism of apigenin-mediated immune modulation has not been fully understood. One of the possible mechanisms of its protective effects is the down-regulation of inflammatory responses. In this study, we used cells from the human mast cell line (HMC-1) to investigate this effect. Apigenin significantly inhibits the inductive effect of phorbol 12-myristate 13-acetate (PMA) plus A23187 on the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-8, IL-6, and granulocyte-macrophage colony-stimulating factor (GM-CSF). Moreover, apigenin attenuated the cyclooxygenase (COX)-2 expression and intracellular Ca(2+) level. In activated HMC-1 cells, apigenin inhibited the PMA plus A23187-induced activation of nuclear factor (NF)-κB, IκB degradation, and luciferase activity. Furthermore, apigenin suppressed the expression of TNF-α, IL-8, IL-6, GM-CSF, and COX-2 by decreasing the intracellular Ca(2+) level and inhibiting NF-κB activation. These results indicate that apigenin has a potential regulatory effect on inflammatory reactions that are mediated by mast cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apigenin / pharmacology*
  • Calcium / metabolism
  • Cell Line
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Down-Regulation / genetics
  • Granulocyte-Macrophage Colony-Stimulating Factor / antagonists & inhibitors
  • Granulocyte-Macrophage Colony-Stimulating Factor / blood
  • Granulocyte-Macrophage Colony-Stimulating Factor / metabolism
  • Humans
  • Inflammation / drug therapy
  • Inflammation / metabolism
  • Inflammation Mediators / antagonists & inhibitors*
  • Inflammation Mediators / metabolism
  • Interleukin-6 / antagonists & inhibitors
  • Interleukin-6 / metabolism
  • Interleukin-8 / antagonists & inhibitors
  • Interleukin-8 / metabolism
  • Luciferases / metabolism
  • NF-kappa B / antagonists & inhibitors*
  • NF-kappa B / metabolism
  • Signal Transduction / drug effects
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Inflammation Mediators
  • Interleukin-6
  • Interleukin-8
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Apigenin
  • Granulocyte-Macrophage Colony-Stimulating Factor
  • Luciferases
  • Cyclooxygenase 2
  • Calcium