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

机译:金雀异黄素对鸡胚绒毛膜尿囊膜模型中脂多糖诱导的急性炎症的保护作用

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摘要

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 LPSinduced 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 inflammationinduced vascular permeability in chick embryos with immature immune capacities.
机译:炎症是对各种外部刺激的生物学反应,可通过信号传导途径诱导血管通透性。脂多糖(LPS)激活急性炎症反应并诱导炎症介质。金雀异黄素具有抗炎活性,但是,还不清楚金雀异黄素是否在鸡胚的不同发育阶段使用相同的信号通路抑制血管通透性。研究了LPS和染料木黄酮治疗后不同免疫阶段绒毛膜的炎症过程。金雀异黄素在未成熟阶段抑制LPS诱导的鸡胚血管通透性。对LPS诱导的CAM中的LPS诱导的toll样受体4(TLR4)信号通路进行了RTPCR和蛋白质印迹。金雀异黄素减弱了LPS诱导的TLR4途径。在未成熟阶段的胚胎中显示出TLR4途径的不同炎症机制。金雀异黄素可能通过不同的信号通路抑制LPS诱导的炎症反应,并具有与免疫功能不成熟的雏鸡胚胎中炎症诱导的血管通透性相关的强大治疗潜力。

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