Poster Presenter

Isoimperatorin Inhibites Lipopolysaccharide-Induced Inflammatory Responses In RAW 264.7 Macrophages Through Suppression Of NF-kB And ERK Pathway
Taesook Yoon, Myeong Sook Cheon, A Yeong Lee, Byeong Cheol Moon, Jin Mi Chun, Byung Kil Choo, Ho Kyoung Kim
South Korea

Isoimperatorin (4-[(3-Methyl-2-butenyl)oxy]-7H-furo[3,2-g][1]benzopyran-7-one) is one of the major furanocoumarins isolated from the various medicinal herbs. We investigated the effects of isoimperatorin on the activities of cellular signaling molecules that mediate inflammatory responses. Isoimperatorin exhibited the inhibitory effect on the release of NO, PGE2, TNF-α, and IL-1β in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells in a dose-dependent manner, with IC50 values of 38.7 M, 26.7 M, 25.5 M, and 20.5 M, respectively. In addition, isoimperatorin significantly suppressed LPS-induced mRNA and protein expression of iNOS and COX-2. To further investigate the mechanism responsible for the suppression of inflammatory mediators production by isoimperatorin, the effect of isoimperatorin on LPS-induced activation of NF-κB and MAPKs (ERK, JNK, and p38) was examined. Isoimperatorin inhibited NF-κB activation and IκB-α degradation. Also, isoimperatorin attenuated the activation of ERK. Taken together, these findings indicate that isoimperatorin can be a possible therapeutic agent for inflammation, and that the anti-inflammatory property of isoimperatorin may result from the inhibition of inflammatory mediators, such as NO, PGE2, TNF-α, and IL-1β via suppression of NF-κB- and MAPK-dependent pathways.