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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。
According to the mechanism of occurrence, cerebral edema can be divided into cytotoxic edema and vasogenic edema. The former is the normal permeability of the cell membrane gradient was destroyed leading to water infiltration into the cells, mainly intracellular edema. Aquaporin-4 (AQP4), an astrocyte foot process in perivascular cells, allows water to enter the cell through the blood-brain barrier, and AQP4 knockout significantly reduces fluid accumulation in cytotoxic brain edema models. In contrast, vasogenic edema originates from an AQP-independent mechanism of increased permeability of the blood-brain barrier leading to extracellular fluid buildup. Studies have shown that AQP4 helps to eliminate extracellular fluid. Based on the relationship between AQP4 and the formation and elimination of brain edema, AQP and AQP expression regulators can provide new ideas for the development of therapeutic drugs for brain edema.