Tranilast inhibits interleukin-1β-induced monocyte chemoattractant protein-1 expression in rat mesangial cells

Akihiro Chikaraishi, Junichi Hirahashi, Osamu Takase, Takeshi Marumo, Keiichi Hishikawa, Matsuhiko Hayashi, Takao Saruta

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Monocyte chemoattractant protein-1 (MCP-1), a member of the CC subfamily of chemokines, plays a crucial role in the progression of glomerulonephritis by recruitment of monocytes. Tranilast, a clinically used anti-allergic drug, has been demonstrated to have various anti-inflammatory and anti-proliferative effects, and recently has been reported to prevent restenosis after percutaneous transluminal coronary angioplasty. In this study, we investigated whether tranilast inhibits MCP-1 secretion in mesangial cells. Tranilast inhibited interleukin-1β-induced MCP-1 secretion and mRNA expression in a concentration-dependent manner. Luciferase assay showed that tranilast suppressed interleukin-1β-induced nuclear factor-κB (NF-κB)-dependent transcription. Interleukin-1β-induced Jun N-terminal kinase (JNK) activation was also suppressed selectively by tranilast. These results indicate that tranilast inhibits interleukin-1β-induced MCP-1 production, at least in part, by inhibiting NF-κB activity and that suppression of JNK activation might be involved in the inhibition of MCP-1 production. Tranilast may serve as a new therapeutic agent for glomerulonephritis through anti-chemokine property.

Original languageEnglish
Pages (from-to)151-158
Number of pages8
JournalEuropean journal of pharmacology
Volume427
Issue number2
DOIs
Publication statusPublished - 2001 Sep 14

Keywords

  • MCP-1 (monocyte chemoattractant protein-1)
  • Mesangial cell
  • NF-κB (nuclear factor-κB)
  • Tranilast

ASJC Scopus subject areas

  • Pharmacology

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