Sinapic Acid Inhibits the IL-1β-Induced Inflammation via MAPK Downregulation in Rat Chondrocytes

Inflammation. 2018 Mar;41(2):562-568. doi: 10.1007/s10753-017-0712-4.

Abstract

Osteoarthritis (OA) is a degenerative joint disease frequently seen in the elderly population. Sinapic acid (SA), a commonly found phenolic acid, has been pharmacologically evaluated for its anti-inflammation effects in various studies. To explore its potential therapeutic role for OA, rat chondrocytes were treated with IL-1β (10 ng/ml) with different concentrations of SA in vitro. Our study revealed that SA could inhibit the IL-1β-induced production of nitric oxide (NO) and prostaglandin E2 (PGE2). Consistent with these findings, the increased protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase (Cox)-2 could also be downregulated by SA. Moreover, SA could also suppress the IL-1β-induced expression of matrix metalloproteinase (MMP)-1, MMP-3, MMP-13, and a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) in chondrocytes. Furthermore, our data found that SA could suppress the IL-1β-induced mitogen-activated protein kinase (MAPK) pathway activation. In general, this paper elucidates that sinapic acid inhibits the IL-1β-induced inflammation via MAPK pathways and may be a good agent for the treatment of OA.

Keywords: ADAMTS5; Cox-2; MAPK; MMPs; iNOS; osteoarthritis.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents
  • Cells, Cultured
  • Chondrocytes / cytology
  • Coumaric Acids / pharmacology*
  • Dinoprostone / biosynthesis
  • Down-Regulation / drug effects
  • Inflammation / drug therapy
  • Inflammation / prevention & control*
  • Interleukin-18 / pharmacology
  • Mitogen-Activated Protein Kinases / metabolism*
  • Nitric Oxide / biosynthesis
  • Osteoarthritis / drug therapy
  • Rats

Substances

  • Anti-Inflammatory Agents
  • Coumaric Acids
  • Interleukin-18
  • Nitric Oxide
  • sinapinic acid
  • Mitogen-Activated Protein Kinases
  • Dinoprostone