Anti-inflammatory effects of trans-1,3-diphenyl-2,3-epoxypropane-1-one mediated by suppression of inflammatory mediators in LPS-stimulated RAW 264.7 macrophages.

To assess the potential therapeutic properties of trans-1,3-diphenyl-2,3-epoxypropane-1-one (DPEP), its anti-inflammatory effects were investigated in lipopolysaccharide (LPS)-stimulated mouse macrophage (RAW 264.7) cells. DPEP induced dose-dependent reduction of the protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and concomitant reduction in the production of NO and prostaglandin E(2) (PGE(2)). Additionally, DPEP suppressed the production of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6. We investigated the mechanism by which DPEP inhibits NO and PGE(2) by examining the level of nuclear factor-κB (NF-κB) activation within the mitogen-activated protein kinase (MAPK) pathway, which is an inflammation-induced signaling pathway in RAW 264.7 cells. DPEP inhibited LPS-induced phosphorylation of ERK, JNK, and p38. Furthermore, DPEP inhibited the LPS-induced phosphorylation of inhibitor κB (IκB)-α and NF-κB p50. Taken together, the results of this study demonstrate that DPEP inhibits LPS-stimulated inflammation by blocking the NF-κB and MAPK pathways in macrophages.

Kim KN ，Ko YJ ，Kang MC ，Yang HM ，Roh SW ，Oda T ，Jeon YJ ，Jung WK ，Heo SJ ，Yoon WJ ，Kim D ... -  《-》

Anti-inflammatory effect of Sosihotang via inhibition of nuclear factor-κB and mitogen-activated protein kinases signaling pathways in lipopolysaccharide-stimulated RAW 264.7 macrophage cells.

Sosihotang (SO) is an herbal medication, which has been widely used to treat fever, chill and vomiting due to common cold in east-Asian countries. In this study, to provide insight into the effects of SO on inflammation, we investigated its effect on pro-inflammatory mediator production in RAW 264.7 cells and mouse peritoneal macrophages using lipopolysaccharide (LPS) stimulation. SO significantly inhibited the production of nitric oxide (NO), tumor necrosis factor (TNF)-α and interleukin (IL)-6 as well as gene expression of inducible nitric oxide synthase (iNOS), its synthesizing enzyme. In addition, SO inhibited nuclear factor (NF)-κB activation and suppressed extracellular signal-regulated kinase (ERK), p38 and c- Jun NH(2)-terminal kinase (JNK) mitogen-activated protein kinases (MAPKs) phosphorylation. Furthermore, we found SO suppresses the production of NO and IL-6 in LPS-stimulated peritoneal macrophage cells. High performance liquid chromatography (HPLC) analysis showed SO contains many active anti-inflammatory constituents such as liquiritigenin, baicalin, baicalein, glycyrrhizin and wogonin. We first elucidated the inhibitory mechanism of SO on inflammation induced by LPS in macrophage cells. Our results suggest SO has potential to be developed as a therapeutic agent for various inflammatory diseases.

Oh YC ，Cho WK ，Jeong YH ，Im GY ，Lee KJ ，Yang HJ ，Ma JY ... -  《-》

Nodakenin suppresses lipopolysaccharide-induced inflammatory responses in macrophage cells by inhibiting tumor necrosis factor receptor-associated factor 6 and nuclear factor-κB pathways and protects mice from lethal endotoxin shock.

Rim HK ，Cho W ，Sung SH ，Lee KT ... -  《-》

Sulfuretin isolated from heartwood of Rhus verniciflua inhibits LPS-induced inducible nitric oxide synthase, cyclooxygenase-2, and pro-inflammatory cytokines expression via the down-regulation of NF-kappaB in RAW 264.7 murine macrophage cells.

It has been reported that Rhusverniciflua exhibits anti-inflammatory, anti-oxidant and anti-cancer activities. However, little is known about biological activity of sulfuretin, a flavonoid isolated from R.verniciflua. In the present study, we investigated the anti-inflammatory effect and the underlying molecular mechanisms of sulfuretin in lipopolysaccharide (LPS)-induced RAW 264.7 cells. Sulfuretin dose-dependently reduced the productions of nitric oxide (NO), prostaglandin E(2) (PGE(2)), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1 beta) induced by LPS. Consistent with these findings, sulfuretin significantly suppressed the LPS-induced expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-alpha, and IL-1 beta. In addition, sulfuretin attenuated LPS-induced DNA binding and the transcriptional activities of nuclear factor-kappa B (NF-kappaB), which was accompanied by a parallel reduction of degradation and phosphorylation of inhibitory kappa B-alpha (I kappaB-alpha) and consequently by decreased nuclear translocation of p65 subunit of NF-kappaB. Furthermore, pretreatment with sulfuretin significantly inhibited the LPS-stimulated activation of I kappaB kinase beta (IKK beta). Taken together, these results suggest that the anti-inflammatory effect of sulfuretin in LPS-treated RAW 264.7 macrophages is associated with the suppression of NF-kappaB transcriptional activity via the inhibitory regulation of IKKbeta phosphorylation.

Shin JS ，Park YM ，Choi JH ，Park HJ ，Shin MC ，Lee YS ，Lee KT ... -  《-》

Flower extract of Panax notoginseng attenuates lipopolysaccharide-induced inflammatory response via blocking of NF-kappaB signaling pathway in murine macrophages.

Jung HW ，Seo UK ，Kim JH ，Leem KH ，Park YK ... -  《-》