摘要
目的 探讨血管内皮细胞在动脉粥样硬化形成过程中的损伤机理。方法 复习相关文献 ,对有关进展进行总结分析。结果 各种致病因素造成细胞因子生成增多 ,激活了控制细胞粘附分子表达的核因子 κB ,进而使细胞粘附分子表达增强 ,促进单核细胞 血管内皮细胞为主的粘附形成增多 ,释放大量炎性介质 (氧自由基及蛋白酶等 ) ,不仅直接损伤血管内皮细胞 ,并可以通过免疫机理使大量单核细胞及中性粒细胞与血管内皮细胞粘附结合 ,进一步损伤血管内皮细胞。同时 ,受损的血管内皮细胞由于膜结构的改变引起抗动脉抗体的产生以致补体系统被激活而加重了血管内皮细胞的损伤 ,也促进了动脉粥样硬化的发生和发展。结论 正确认识血管内皮细胞在动脉粥样硬化发生、发展过程中受损机理 。
Objective To summarize the progress on the injury mechanism of vascular endothelial cells in atherosclerosis.Methods The latest progress was reviewed in recent literatures.Results All kinds of etiological factors have activated NF kappa B and cytokines in the development of atherosclerosis, which lead to expression of cell adhesive molecules and adhesion of monocytes to vascular endothelial cells.A variety of inflammatory mediums are released, which can directly damage endothelial cells.Besides, the inflammatory mediums make monocytes and neutrophils attach to endothelial cells by immune mechanisms, which injure the endothelial cells more severely. Meanwhile the damaged membrance structure leads to the production of AECA which activates the complementary system. Then the vascular endothelial cell injury is aggravated and the development of atherosclerosis accelerated. Conclusion It is very important to recognize the injury mechanism of vascular endothelial cells in the development of atherosclerosis for prevention and treatment of atherosclerosis.
出处
《中国普外基础与临床杂志》
CAS
2004年第4期325-327,共3页
Chinese Journal of Bases and Clinics In General Surgery
