ObjectivesThe aim of this study was to investigate anti-inflammatory activity of Mugi-hwan (MGH) Water Extract. MethodsCells were treated with 2 ug/ml of LPS 1 hour prior to the addition of MGH. Cell viability was measured by MTS assay. The production...
ObjectivesThe aim of this study was to investigate anti-inflammatory activity of Mugi-hwan (MGH) Water Extract. MethodsCells were treated with 2 ug/ml of LPS 1 hour prior to the addition of MGH. Cell viability was measured by MTS assay. The production of NO was determined by reacting cultured medium with Griess reagent. The expression of COX-2, iNOS and MAPKs was investigated by Western blot, RT-PCR. The content of level of cytokines (PGE2, IL-6, in media from LPS-stimulated Raw 264.7 cells was analyed by ELISA kit. ResultsMGH inhibited the production of NO, PGE2, IL-6 as well as the expressions of iNOS, COX-2 in the murine macrophage, RAW 264.7 cells. MGH also had suppression effects of LPS induced MAPKs activation. ConclusionsThese results suggest that MGH has an anti-inflammatory therapeutic potential, which may result from inhibition of MAPK phosphorylation, thereby decreasing the expression of pro-inflammatory genes. (J Korean Med Rehab 2013;23(3):27-35) ObjectivesThe aim of this study was to investigate anti-inflammatory activity of Mugi-hwan (MGH) Water Extract. MethodsCells were treated with 2 ug/ml of LPS 1 hour prior to the addition of MGH. Cell viability was measured by MTS assay. The production of NO was determined by reacting cultured medium with Griess reagent. The expression of COX-2, iNOS and MAPKs was investigated by Western blot, RT-PCR. The content of level of cytokines (PGE2, IL-6, in media from LPS-stimulated Raw 264.7 cells was analyed by ELISA kit. ResultsMGH inhibited the production of NO, PGE2, IL-6 as well as the expressions of iNOS, COX-2 in the murine macrophage, RAW 264.7 cells. MGH also had suppression effects of LPS induced MAPKs activation. ConclusionsThese results suggest that MGH has an anti-inflammatory therapeutic potential, which may result from inhibition of MAPK phosphorylation, thereby decreasing the expression of pro-inflammatory genes. (J Korean Med Rehab 2013;23(3):27-35)