Biochanin-A antagonizes the interleukin-1β-induced catabolic inflammation through the modulation of NFκB cellular signaling in primary rat chondrocytes

Biochem Biophys Res Commun. 2016 Sep 2;477(4):723-730. doi: 10.1016/j.bbrc.2016.06.126. Epub 2016 Jun 27.

Abstract

Biochanin-A, a phytoestrogen derived from herbal plants, protected from the IL-1β-induced loss of proteoglycans through the suppression of matrix degrading enzymes such as matrix metalloproteinase (MMP)-13, MMP-3, MMP-1, and ADAMTS-5 in primary rat chondrocytes and the knee articular cartilage. It also suppressed the expression of IL-1β-induced catabolic factors such as nitric oxide synthase 2, cyclooxygenase-2, prostaglandin E2, and inflammatory cytokines. Furthermore, biochanin-A suppressed the IL-1β-induced phosphorylation of NFκB, and inhibited its nuclear translocation in primary rat chondrocytes. These results indicate that biochanin-A antagonizes the IL-1β-induced catabolic effects through its anti-inflammatory activity that involves the modulation of NFκB signaling.

Keywords: Anti-catabolic effects; Biochanin-A; Inflammation; Osteoarthritis; Phytoestrogen.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / administration & dosage
  • Cells, Cultured
  • Chondrocytes / drug effects
  • Chondrocytes / immunology*
  • Dose-Response Relationship, Drug
  • Genistein / administration & dosage*
  • Interleukin-1beta / immunology*
  • Metabolism / drug effects
  • NF-kappa B / immunology*
  • Osteoarthritis / drug therapy*
  • Osteoarthritis / immunology*
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction / immunology

Substances

  • Anti-Inflammatory Agents
  • Interleukin-1beta
  • NF-kappa B
  • Genistein
  • biochanin A