Monascus-fermented metabolite monascin suppresses inflammation via PPAR-γ regulation and JNK inactivation in THP-1 monocytes

Wei Hsuan Hsu, Bao Hong Lee, Te Han Liao, Ya Wen Hsu, Tzu Ming Pan

Research output: Contribution to journalArticlepeer-review

40 Citations (Scopus)

Abstract

Fermentation products of the fungus Monascus offer valuable therapeutic benefits and have been used extensively for centuries in Asia. The aim of this study is to investigate the inhibitory effect of the Monascus-fermented metabolite monascin (MS) on the molecular mechanism of ovalbumin (OVA)-induced inflammation in the human THP-1 monocyte cell line. We found that 1, 5, and 25μM of MS significantly attenuated several proinflammatory mediators, including inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression as well as nitric oxide (NO) and prostaglandin E 2 (PGE 2) formation caused by OVA stimulation. Further, 5 and 25μM of MS significantly reduced the generation of tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) at both the protein and mRNA levels. MS (5 and 25μM) decreased OVA-induced phosphorylation of mitogen-activated protein kinase (MAPK) c-Jun NH 2-terminal kinase (JNK), but not that of extracellular signal-regulated kinase (ERK) or p38 kinase. We used the peroxisome proliferator activated receptor-γ (PPAR-γ) antagonist GW9662 to show that MS inhibit JNK phosphorylation through increased expression of PPAR-γ Thus, the metabolites from Monascus fermentation may serve as a dietary source of anti-inflammatory agents.

Original languageEnglish
Pages (from-to)1178-1186
Number of pages9
JournalFood and Chemical Toxicology
Volume50
Issue number5
DOIs
Publication statusPublished - 2012 May 1

All Science Journal Classification (ASJC) codes

  • Food Science
  • Toxicology

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