肿瘤坏死因子-α通过内皮型一氧化氮合酶和小凹蛋白-1介导内皮细胞功能失调的研究

摘要

血管内皮细胞功能失调是致动脉粥样硬化形成的重要机制之一。其中，内皮型一氧化氮合酶和小凹蛋白-1是调节脂质物质摄取和炎症细胞跨内皮迁移的重要蛋白。肿瘤坏死因子-α为多效性促炎症反应细胞因子，可通过核因子-κB信号通路下调内皮型一氧化氮合酶表达，上调小凹蛋白-1表达，诱导内皮细胞胞吞转运作用失衡和炎症细胞跨内皮迁移，促使局部血管斑块形成。现就肿瘤坏死因子-α通过核因子-κB信号通路诱导血管内皮功能失调的机制做一简要综述。%Endothelium dysfunction plays an crucial role in the development of atherosclerosis .Endothelial nitric oxide synthase ( eNOS) and caveolin-1 are important proteins in modulating lipids uptake and inflammatory cell tranendothelial migration .Tumor nuclear factor-αas pleiotropic proinflammatory cytokine ,mediates eNOS and caveolin-1 expression ,elicits endothelium dysfunction via nuclear factor-κB signaling pathway .Here we describe the detailed mechanisms of tumor nuclear factor-αmodulated endothlium dysfunction via nuclear fac-tor-κB pathway .