Protection of vessel permeability by genistein against lipopolysaccharide induced acute inflammation in a chick embryo chorioallantoic membrane model

Abstract

Inflammation is a biological response to various external stimuli that induces vascular permeability via signaling pathways. Lipopolysaccharide (LPS) activates the acute inflammatory response and induces inflammatory mediators. Genistein has an anti-inflammation activity, however, whether genistein inhibits vascular permeability using the same signaling pathways at different development stages in chick embryos is unclear. Inflammatory processes in the chorioallantoic membrane (CAM) after LPS and genistein treatments at different immune stages were investigated. Genistein suppresses LPS-induced vascular permeability in chick embryos at the immature stage. RTPCR and western blotting were performed for LPS-induced toll-like receptor 4 (TLR4) signaling pathways in the CAM. The LPS-induced TLR4 pathways are attenuated by genistein. Different inflammation mechanisms in TLR4 pathways are shown in embryos in the immature stage. Genistein probably inhibits the LPS-induced inflammatory response through different signaling pathways and has a strong therapeutic potential associated with inflammation-induced vascular permeability in chick embryos with immature immune capacities.