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.
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NO PGE(2) DPEP DPEP DPEP trans-1,3-diphenyl-2,3-epoxypropane-1-one p50 NF-κB MAPK inducible nitric oxide synthase DPEP iNOS cyclooxygenase-2 COX-2 cytokines tumor necrosis factor-α TNF-α interleukin (IL)-1β IL-6 nuclear factor-κB NF-κB DPEP mitogen-activated protein kinase MAPK ERK JNK p38 inhibitor κB (IκB)-α NF-κB nitric oxide NO prostaglandin E(2) PGE(2) DPEP trans-1,3-diphenyl-2,3-epoxypropane-1-one DPEP