Rengyolone inhibits inducible nitric oxide synthase expression and nitric oxide production by down-regulation of NF-κB and p38 MAP kinase activity in LPS-stimulated RAW 264.7 cells

Jin Hee Kim, Dong Hyun Kim, Seung Hwa Baek, Ho Jae Lee, Mee Ree Kim, Ho Jeong Kwon, Choong Hwan Lee

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Nitric oxide (NO) is recognized as a mediator and regulator of inflammatory responses. Rengyolone, a cyclohexylethanoid isolated from the fruits of Forsythia koreana, exhibits anti-inflammatory activity with unknown mechanism. In this study, we found that rengyolone has a strong inhibitory effect on the production of nitric oxide (NO) and tumor necrosis factor-α (TNF-α). Rengyolone also inhibited inducible nitric oxide synthase (iNOS) gene expression and cyclooxygenase 2 (COX-2) by lipopolysaccharide (LPS). In order to explore the mechanism responsible for the inhibition of iNOS gene expression by rengyolone, we investigated its effect on LPS-induced nuclear factor-κB (NF-κB) activation. The LPS-induced DNA binding activity of NF-κB was significantly inhibited by rengyolone, and this effect was mediated through inhibition of the degradation of inhibitory factor-κBα and phosphorylation of p38 MAP kinase. Furthermore, rengyolone suppressed the expression of ICE protein in IL-1β-treated D10S cells. Taken together, these results suggest that rengyolone attenuates the inflammation through inhibition of NO production and iNOS expression by blockade of NF-κB and p38 MAPK activation in LPS-stimulated RAW 264.7 cells.

Original languageEnglish
Pages (from-to)1198-1205
Number of pages8
JournalBiochemical Pharmacology
Issue number8
Publication statusPublished - 2006 Apr 14


All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Pharmacology

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