Casticin protects against IL-1β-induced inflammation in human osteoarthritis chondrocytes

Eur J Pharmacol. 2019 Jan 5:842:314-320. doi: 10.1016/j.ejphar.2018.10.051. Epub 2018 Nov 2.

Abstract

Casticin, an active compound isolated from Vitex rotundifolia L., was reported to possess anti-inflammatory activity. However, the effect of casticin on inflammatory response in human osteoarthritis (OA) chondrocytes remains unclear. In the current study, we examined the anti-inflammatory effects of casticin on chondrocytes exposed to interleukin-1β (IL-1β). Our results demonstrated that casticin treatment significantly improved cell viability in chondrocytes exposed to IL-1β. Casticin significantly inhibited IL-1β-induced NO and PGE2 production, and iNOS and COX-2 expression in human OA chondrocytes. It also suppressed the levels of TNF-α and IL-6, as well as decreased production of MMP-3, MMP-13, ADAMTS-4 and ADAMTS-5 in IL-1β-stimulated chondrocytes. Furthermore, casticin prevented IL-1β-induced NF-κB activation in chondrocytes. Taken together, these findings showed that casticin attenuates inflammatory responses in chondrocytes stimulated with IL-1β, possibly through the NF-κB signaling pathway. Thus, casticin may serve as a potential anti-inflammatory agent in the treatment of OA.

Keywords: Casticin; IL-1β; Inflammation; NF-κB pathway; Osteoarthritis (OA).

MeSH terms

  • ADAMTS Proteins / biosynthesis
  • Cell Survival / drug effects
  • Chondrocytes / drug effects*
  • Chondrocytes / metabolism
  • Chondrocytes / pathology*
  • Cyclooxygenase 2 / genetics
  • Cytoprotection / drug effects
  • Dinoprostone / biosynthesis
  • Flavonoids / pharmacology*
  • Gene Expression Regulation, Enzymologic / drug effects
  • Humans
  • Inflammation / chemically induced
  • Inflammation / metabolism
  • Inflammation / pathology
  • Inflammation / prevention & control
  • Interleukin-1beta / pharmacology*
  • Interleukin-6 / metabolism
  • Matrix Metalloproteinases / biosynthesis
  • Nitric Oxide / biosynthesis
  • Nitric Oxide Synthase Type II / genetics
  • Osteoarthritis / chemically induced
  • Osteoarthritis / metabolism
  • Osteoarthritis / pathology*
  • Osteoarthritis / prevention & control*
  • Signal Transduction / drug effects
  • Transcription Factor RelA / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Flavonoids
  • Interleukin-1beta
  • Interleukin-6
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • casticin
  • Nitric Oxide Synthase Type II
  • Cyclooxygenase 2
  • ADAMTS Proteins
  • Matrix Metalloproteinases
  • Dinoprostone