Biochanin A inhibits lipopolysaccharide-induced inflammation in human umbilical vein endothelial cells

Life Sci. 2015 Sep 1:136:36-41. doi: 10.1016/j.lfs.2015.06.015. Epub 2015 Jul 2.

Abstract

Aim: Biochanin A, an isoflavone isolated from red clover, cabbage or alfalfa, has been reported to have anti-inflammatory activity. However, the effects of biochanin A on vascular inflammation have not been investigated. In this study, we investigate the anti-inflammatory effects of biochanin A on lipopolysaccharide (LPS)-induced inflammatory response in human umbilical vein endothelial cells (HUVEC cells).

Main methods: The HUVEC cells were treated with biochanin A for 12h before exposure to LPS. The expression of ECAMs, including VCAM-1, ICAM-1, E-selectin, NF-κB and PPAR-γ was detected by Western blotting. The expression of cytokines TNF-α and IL-8 was detected by ELISA.

Key findings: The results showed that biochanin A inhibited LPS-induced TNF-α and IL-8 production. Meanwhile, biochanin A also suppressed VCAM-1, ICAM-1, and E-selectin expression induced by LPS. We also found that biochanin A inhibited NF-κB activation induced by LPS. Furthermore, biochanin A could activate PPAR-γ and the anti-inflammatory effects of biochanin A can be reversed by GW9662, a specific antagonist for PPAR-γ.

Significance: In conclusion, the anti-inflammatory effect of biochanin A is associated with activating PPAR-γ, thereby attenuating NF-κB activation and LPS-induced inflammatory response. These findings suggest that biochanin A may be a therapeutic agent for inflammatory cardiovascular disease.

Keywords: Biochanin A; Cytokine; Human umbilical vein endothelial cells; NF-κB; PPAR-γ.

MeSH terms

  • Anti-Inflammatory Agents / pharmacology*
  • Cell Survival / drug effects
  • Cells, Cultured
  • E-Selectin / genetics
  • E-Selectin / metabolism
  • Genistein / pharmacology*
  • Human Umbilical Vein Endothelial Cells / drug effects
  • Human Umbilical Vein Endothelial Cells / immunology*
  • Humans
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism
  • Interleukin-8 / biosynthesis
  • Lipopolysaccharides / pharmacology
  • NF-kappa B / metabolism
  • PPAR gamma / metabolism
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Vascular Cell Adhesion Molecule-1 / genetics
  • Vascular Cell Adhesion Molecule-1 / metabolism

Substances

  • Anti-Inflammatory Agents
  • E-Selectin
  • Interleukin-8
  • Lipopolysaccharides
  • NF-kappa B
  • PPAR gamma
  • SELE protein, human
  • TNF protein, human
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1
  • Genistein
  • biochanin A