水通道蛋白-4与脑水肿  

Aquaporin-4 and Brain Edema

作　　者：杨晓波[1] 宋水江[1] 

机构地区：[1]浙江大学医学院附属第二医院神经内科,杭州310009

出　　处：《国际脑血管病杂志》2006年第6期448-451,共4页International Journal of Cerebrovascular Diseases

摘　　要：根据发生机制,脑水肿可分为细胞毒性水肿和血管源性水肿。前者是细胞膜正常渗透梯度被破坏导致水渗透性内流进入细胞,主要为细胞内水肿。血管周围星形胶质细胞足突的水通道蛋白-4(AQP4)可使水通过血脑屏障进入细胞,AQP4基因敲除可显著减少细胞毒性脑水肿模型的液体积聚。相反,血管源性水肿源于一种不依赖AQP的血脑屏障通透性增高机制,导致细胞外液体积聚。研究表明,AQP4有助于消除细胞外液体。基于AQP4与脑水肿形成和消除的关系,AQP和AQP表达调节剂可为脑水肿治疗药物的开发提供新的思路。Brain edema can be divided into cytotoxic edema and vasogenic edema, according to its pathogenesis. Cytotoxic edema results in osmotic water flowing into cells after the normal osmotic gradients of cell membrane being disrupted, and it is mainly intracellular edema. Aquaporin-4 （AQP4） water channels in the foot processes of perivascular astrocytes facilitate water movement from the vascular space across the blood-brain barrier （BBB） into cells. AQP4 deletion significantly reduced the accumulation of intracellular fluid in mice. On the contrary, vasogenic edema originates from an aquaporin-independent mechanism involving increased BBB permeability, resulting in the extracellular fluid accumulation. Studies have suggested that AQP4 facilitates the clearance of extracellular fluid. In view of the relations between AQP4 and edema formation and clearance, AQP and its expression regulators may provide new approaches for the development of drugs for the treatment of brain edema.

关 键 词：水通道蛋白-4 脑水肿 血脑屏障 

分 类 号：R741[医药卫生—神经病学与精神病学]