白细胞介素4与动脉粥样硬化  

Interleukin-4 and Atherosclerosis

作　　者：谈春芝[1,2] 吴洁[2] 唐朝克[1] 

机构地区：[1]南华大学心血管病研究所生命科学研究中心,湖南省衡阳市421001 [2]南华大学附属第一医院心内科,湖南省衡阳市421001

出　　处：《中国动脉硬化杂志》2011年第2期155-159,共5页Chinese Journal of Arteriosclerosis

基　　金：国家自然科学基金(30470720);湖南省自然科学基金(06jj5058)项目资助

摘　　要：血管内皮损伤与功能紊乱是动脉粥样硬化等心血管疾病的启动和进展因素。已有大量的研究表明,内皮细胞的氧化及炎症在动脉粥样硬化起始和进展中发挥重要作用。越来越多的证据表明白细胞介素4能够经由氧化应激上调炎性介质,如细胞因子、趋化因子和血管内皮细胞黏附分子。同时白细胞介素4能通过多种信号通路加速细胞凋亡,促进细胞内皮更新,这能够导致血管内皮功能失调。这些研究将极大可能为预防和治疗血管炎症性疾病如动脉粥样硬化等提供靶点及方向。Vascular endothelial cell injury or dysfunction has been implicated in the onset and progression of cardiovascular diseases including atherosclerosis.Numerous studies have indicated that endothelial cells oxidative and inflammation play an important role in initiation and progress of atherosclerosis.More and more studies have demonstrated that interleukin-4 can increase oxidative stress by inflammatory mediators such as cytokines,chemokines and endothelial cell adhesion molecule.Interleukin-4 can accelerate apoptosis and promote endothelial cell updates through a variety of signaling pathway,which can lead to vascular endothelial dysfunction.These studies will most likely provide new targets or direction for the prevention and treatment of vascular inflammatory diseases such as atherosclerosis.

关 键 词：白细胞介素4 动脉粥样硬化 氧化应激 细胞凋亡 黏附分子 趋化因子 

分 类 号：R363[医药卫生—病理学]