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Anti-inflammatory Effects of the Methanol Extract of Polytrichum Commune via NF-κB Inactivation in RAW 264.7 Macrophage Cells

  • Cho, Woong (Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung-Hee University) ;
  • Park, Seung-Jae (Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung-Hee University) ;
  • Shin, Ji-Sun (Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung-Hee University) ;
  • Noh, Young-Su (Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung-Hee University) ;
  • Cho, Eu-Jin (Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung-Hee University) ;
  • Nam, Jung-Hwan (Highland Agricultural Institute, Rural Development Adminstration) ;
  • Lee, Kyung-Tae (Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung-Hee University)
  • Published : 2008.12.31

Abstract

As an attempt to search for bioactive natural products exerting anti-inflammatory activity, we evaluated the effects of the methanol extract of Polytrichum commune Hedw (PCM) (Polytrichaceae) on lipopolysaccharide (LPS)-induced nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$) and pro-inflammatory cytokines release in murine macrophage cell line RAW 264.7. PCM potently inhibits the production of NO, $PGE_2$, tumor necrosis factor (TNF)-$\alpha$ and interleukin (IL)-6. Consistent with these results, PCM also concentration-dependently inhibited LPS-induced inducible NO synthase (iNOS) and cyclooxygase (COX)-2 at the protein levels, and iNOS, COX-2, TNF-$\alpha$ and IL-6 at the mRNA levels without an appreciable cytotoxic effect on RAW 264.7 macrophag cells. Furthermore, PCM inhibited LPS-induced nuclear factor-kappa B (NF-$\kappa$B) activation as determined by NF-$\kappa$B reporter gene assay, and this inhibition was associated with a decrease in the nuclear translocation of p65 and p50 NF-$\kappa$B. Taken together, these results suggest that PCM may play an anti-inflammatory role in LPS-stimulated RAW 264.7 macrophages through the inhibitory regulation of iNOS, COX-2, TNF-$\alpha$ and IL-6 via NF-$\kappa$B inactivation.

Keywords

References

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