吸烟和血清脂蛋白相关磷脂酶A_2水平与冠心病的研究进展  

Cigarette Smoking,Serum Level of Lipoprotein Associated Phospholipase A_2 and Coronary Heart Disease

作　　者：唐春男 陶志刚[1] 

机构地区：[1]青岛大学医学院附属烟台毓璜顶医院心内科,山东烟台264000

出　　处：《医学综述》2015年第23期4272-4274,共3页Medical Recapitulate

摘　　要：吸烟是冠状动脉粥样硬化性心脏病(冠心病)重要的危险因素,但其导致冠心病的具体机制尚不明了。血清脂蛋白相关磷脂酶A_2(LP-PLA_2)可快速降解氧化低密度脂蛋白(ox-LDL),生成强促炎因子,增强局部血管炎症反应,与冠心病的发生、粥样斑块的稳定性、冠状动脉病变程度均密切相关。而吸烟可增强机体氧化应激、增加低密度脂蛋白(LDL)的氧化,进而上调单核细胞内LP-PLA_2的表达,使LP-PLA_2总量及活性增高,导致局部血管的炎症反应增强,促进冠心病的发生、发展。Smoking is an important independent risk factor for coronary heart disease （CHD）, but the specific pathogenesis is still unknown. Lipoprotein associated phospholipase A2 （ LP-PLA2 ） is a kind of phospholipase which is highly vascular inflammation specific, can degrade oxidized low density lipoprotein rapidly, generate strong proinflammatory factors, enhance the local vascular inflammation, and is closely related with the oceurrence of CHD,the stability of atherosclerotic plaque and coronary artery lesion degree. Smoking can enhance the oxidative stress,increases the oxidation of LDL, therefore upregulate the expression of LP-PLA2 in mononuclear cells, and elevate the mass and activity of serum LP-PLA2 , promote vascular inflammation, and eventually result in the occurrence and development of CHD.

关 键 词：冠心病 吸烟 氧化应激 炎症反应 脂蛋白相关磷脂酶A2 

分 类 号：R541.4[医药卫生—心血管疾病]