AQP4基因沉默对脑水肿的影响及影像改变

摘要

The mechanism of cerebral edema is complex. The intracellular Ca2+overload, free radical damage, and reduction of Na +~-K +~-ATPase activity in cell membrane are associated with the formation of brain edema, but these mechanisms hardly explain the occurrence of cerebral edema exactly. In recent years, the study of aquaporin4 (AQP4) at molecular level brings a breakthrough to make the mechanism of cerebral edema clear. A number of experimental studies have shown that AQP4 is closely related to the formation of cerebral edema. It has been reported that AQP4 gene silencing which reduces the expression of AQP4 can reduce the extent of brain edema. The purposes of this article were to explore the effects of AQP4 gene silencing on brain edema and corresponding imaging changes and to provide theoretical basis for the diagnosis and treatment of cerebral edema.%脑水肿的发生机制十分复杂，细胞内Ca2+超载、自由基损害、细胞膜Na+,K+-ATP酶活性降低等均与脑水肿的形成相关，但这些机制并不能很好地解释脑水肿的发生。近年来分子水平上水通道蛋白4（AQP4）的研究为探索脑水肿的发生机制带来了突破性进展。AQP4参与脑水肿的形成。AQP4基因沉默降低了AQP4的表达并能减轻脑水肿的程度。就AQP4基因沉默对脑水肿的影响及影像改变进行综述，以期为脑水肿的诊治提供有效的理论依据。