Anti-Inflammatory Effect of Sedum takesimense Nakai Water Extract in RAW 264.7 Cells
2016
Jang, J.H., National Development Institute of Korean Medicine, Jangheung, Republic of Korea | Jung, H.K., National Development Institute of Korean Medicine, Jangheung, Republic of Korea | Ko, J.H., National Development Institute of Korean Medicine, Jangheung, Republic of Korea | Sim, M.O., National Development Institute of Korean Medicine, Jangheung, Republic of Korea | Woo, K.W., National Development Institute of Korean Medicine, Jangheung, Republic of Korea | Kim, T.M., National Development Institute of Korean Medicine, Jangheung, Republic of Korea | Lee, K.H., National Development Institute of Korean Medicine, Jangheung, Republic of Korea | Ahn, B.K., National Development Institute of Korean Medicine, Jangheung, Republic of Korea | Cho, H.W., National Development Institute of Korean Medicine, Jangheung, Republic of Korea | Cho, J.H., National Development Institute of Korean Medicine, Jangheung, Republic of Korea | Jung, W.S., National Development Institute of Korean Medicine, Jangheung, Republic of Korea
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 ㎍/㎖. 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)-1beta‚ and IL-6 were also reduced. Conclusions: These results suggest that the down regulation of iNOS, COX-2, TNF-alpha, IL-1beta‚ and IL-6 expression by SKLC are mediated by the down regulation of nuclear factor-κB (NF-κB) activity, a transcription factor necessary for pro-inflammatory mediators. This might be the mechanism underlying the anti-inflammatory effects of SKLC.
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