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Anti-Inflammatory Effect of Sedum takesimense Nakai Water Extract in RAW 264.7 Cells

섬기린초 물 추출물의 마우스 대식세포에서 항염증 효능

  • Jang, Ji Hun (National Development Institute of Korean Medicine) ;
  • Jung, Ho Kyung (National Development Institute of Korean Medicine) ;
  • Ko, Jae Hyung (National Development Institute of Korean Medicine) ;
  • Sim, Mi Ok (National Development Institute of Korean Medicine) ;
  • Woo, Kyeong Wan (National Development Institute of Korean Medicine) ;
  • Kim, Tae Muk (National Development Institute of Korean Medicine) ;
  • Lee, Ki Ho (National Development Institute of Korean Medicine) ;
  • Ahn, Byeong Kwan (National Development Institute of Korean Medicine) ;
  • Cho, Hyun Woo (National Development Institute of Korean Medicine) ;
  • Cho, Jung Hee (National Development Institute of Korean Medicine) ;
  • Jung, Won Seok (National Development Institute of Korean Medicine)
  • Received : 2016.04.21
  • Accepted : 2016.06.10
  • Published : 2016.06.30

Abstract

Background: Sedum takesimense Nakai has been used as folk medicine in Korea. The present study aimed to determine the biological activity of S. takesimense by investigating the anti-inflammatory effects of S. takesimense water extract (SKLC) on the lipopolysaccharide-induced inflammatory response in RAW 264.7 cells. Methods and Results: Cytotoxicity of SKLC on RAW 264.7 cells was determinded by performing MTS assay was found to have no cytotoxic effect on RAW 264.7 cells at a concentration range of $62-500{\mu}g/m{\ell}$. Further, pretreatment of SKLC inhibited lipopolysaccharide-induced nitric oxide (NO) production in a dose-dependent manner. To determined the inhibitory mechanisms of SKLC on inflammatory mediators, we assessed the inducible nitric oxide synthase (iNOS) and cyclooxygnease-2 (COX-2) pathways. The activities of these pathways were decreased in a dose-dependent manner by SKLC. The production of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin $(IL)-1{\beta}$, and IL-6 were also reduced. Conclusions: These results suggest that the down regulation of iNOS, COX-2, TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 expression by SKLC are mediated by the down regulation of nuclear factor-${\kappa}B$ (NF-${\kappa}B$) activity, a transcription factor necessary for pro-inflammatory mediators. This might be the mechanism underlying the anti-inflammatory effects of SKLC.

Keywords

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