脑水肿是指脑内水分增加导致脑容积增大的一种病理现象,是脑组织对各种致病因素的反应。颅内损伤、缺血、缺氧、炎症、脑代谢障碍、肿瘤以及中毒都会引起脑水肿。脑水肿可导致颅内压的升高,当颅内压升高到一定程度时,脑组织就会发生功能和结构的损害,严重者导致脑死亡。先前对脑水肿发病机制的研究包括血脑屏障学说、钙离子学说、脑微循环障碍学说、脑细胞代谢障碍等。但是近年的研究表明脑水肿的发生与水通道蛋白4、基质金属蛋白酶、紧密连接蛋白、炎性细胞因子等密切相关。本文就脑水肿发生的分子机制进行综述。
Cerebral edema is a pathological sign of increased brain volume induced by accumulation of fluid in the brain,and it is the response of brain tissues to a variety of pathogenic factors. Intracranial injury,ischemia,hypoxia,inflammation,cerebral dysmetabolism,brain tumor and poisoning can all cause brain edema. Brain edema can induce elevation of intracranial pressure,and functional and structural injuries can be found when level of intracranial pressure increases to a certain degree,and it also can lead to brain death. The previous study for the mechanism of cerebral edema includes blood-brain barrier theory,calcium ion theory,cerebral microcirculation disturbance theory and so on. The study of recent years has shown that incidence of cerebral edema closely relates to aquaporin-4( AQP4),matrix metalloproteinases( MMPs),tight junction( TJ) protein and inflammatory cytokines. This paper summarizes the molecular mechanisms of cerebral edema.