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同型半胱氨酸是动脉粥样硬化形成的一种独立危险因素,它可以通过诱导细胞粘附分子和趋化因子的表达促进动脉粥样硬化形成的早期事件一单核细胞粘附于血管内皮细胞,并迁入内皮摄取脂质转化为泡沫细胞的发生。细胞因子等相关因素可通过不同的转录因子与途径调节这一过程,其中对NF—kB的作用有较深入的研究。高同型半胱氨酸血症患者的血清中亦可检出增高的可溶性细胞粘附分子和趋化因子。因此对粘附分子和趋化因子在同型半胱氨酸诱导动脉粥样硬化形成过程中的作用机制的探讨具有重要意义。
Homocysteine is an independent risk factor for the development of atherosclerosis. It promotes the development of atherosclerosis by inducing the expression of cell adhesion molecules and chemokines. Monocyte adhesion to vascular endothelium Cells and into the endothelium uptake of lipids into foam cells. Cytokines and other related factors through different transcription factors and pathways to regulate this process, of which the role of NF-kB in-depth study. Patients with hyperhomocysteinemia also detect elevated levels of soluble cell adhesion molecules and chemokines. Therefore, the adhesion molecules and chemokines in homocysteine-induced atherosclerosis formation mechanism of action is of great significance.