缺氧肺动脉高压发病机制研究进展:15-LO/15-HETE的作用  

Advances in research on the mechanism of hypoxic pulmonary hypertension:role of 15-LO/15-HETE

作　　者：郑晓东[1] 朱大岭[1,2] 

机构地区：[1]哈尔滨医科大学药学院 [2]黑龙江省生物医药工程重点实验室,黑龙江哈尔滨150086

出　　处：《中国药理学通报》2009年第2期157-160,共4页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No30370578;30470752)

摘　　要：缺氧肺动脉高压(HPH)以急性缺氧肺动脉收缩(HPV)和慢性缺氧导致的肺血管床重构(HPVR)引起的肺动脉压持续升高为特征的临床常见病症。参与HPH的中介因子很多,但没有一种可以完整地阐述其发病机制。本实验室前期工作发现缺氧可使肺血管15-脂酯氧化酶(15-LO)表达升高,后者催化花生四烯酸,生成15-羟基二十碳四烯酸(15-HETE)。研究发现15-LO/15-HETE参与HPV与HPVR的众多过程,提示15-LO/15-HETE可能是HPH发病过程的一个中介因子。对15-LO/15-HETE研究将更好地阐述HPH的发病机制,寻找更有效的临床治疗靶点。Hypoxie puhnonary hypertension （HPH） is a common disease featured by acute hypoxic pulmonary vasoconstriction （HPV） and chronic hypoxic pulmonary vascular remolding （HPVR） leading to the sustained increasing of pulmonary artery pressure. There are many mediators involved in the HPH but none can illustrate it successfully. Primary work has found 15-lipoxygenase （15-LO） and its catalyzed production 15-hydroxyeicosatetraenoic acid （15-HETE） （from arachidonic acid） are upregulated in pulmonary vascular when exprosed to hypoxia. And it has been tound 15-LO/15-HETE involved in many processes of both the HPV and HPVR, indicating 15-LO/15-HETE may be an important mediator of HPH. Advances research on 15-LO/ 15-HETE may illustrate the mechanism of HPH, and will give some message in looking for a potential clinical target of HPH.

关 键 词：缺氧肺动脉高压 15-脂酯氧化酶 15-羟基二十碳四 烯酸 缺氧肺动脉收缩 缺氧肺血管重构 

分 类 号：R-05[医药卫生] R322.121