Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2580385 | Chemico-Biological Interactions | 2014 | 7 Pages |
•DDP inhibited the releases of proinflammatory mediators in LPS-stimulated macrophages.•DDP blockade the NF-κB and MAPK activation induced by LPS in macrophages.•DDP improves survival in experimental endotoxin shock.
Activated macrophages mediate inflammation, as they release nitric oxide and pro-inflammatory cytokines in various inflammatory diseases. Suppressing macrophage activation may alleviate inflammatory processes. Here, we report that (E)-3-(3,4-dihydroxy-2-methoxyphenyl)-1-(2,4-dihydroxyphenyl)prop-2-en-1-one (DDP), a novel licochalcone B derivative compound, inhibits inflammatory reactions in macrophages and protects mice from endotoxin shock. In vitro experiments showed that DDP suppressed the generation of nitric oxide and pro-inflammatory cytokines by suppressing the activation of nuclear factor-κB and activator protein-1 and simultaneously inhibited its upstream inflammatory signaling cascades in lipopolysaccharide in RAW264.7 cells. In an animal model, DDP protected BALB/c mice from lipopolysaccharide-induced endotoxin shock, possibly through inhibition of the production of inflammatory cytokines. DDP inhibited the production of inflammatory mediators and may be a potential target for treatment of various inflammatory diseases.