中文摘要：

目的：研究水通道蛋白4（AQP4）在脑出血后脑水肿形成中的作用。方法：以AQP4基因敲除（AQP4^-/-）小鼠为研究对象,分别在AQP4^＋/＋和野生型（AQP4^-/-）小鼠右侧基底节区立体定向注入5μL自体全血建立脑出血模型。比较两组小鼠脑出血后神经功能缺损、脑含水量、血肿周围组织脑比重、伊文思蓝漏出量及脑组织毛细血管超微结构间的差异。结果：脑出血后AQP4^＋/＋小鼠脑内AQP4蛋白表达量显著增高。AQP4基因的缺失加剧了脑出血神经功能缺损及患侧大脑半球的含水量,降低了血肿周围组织的脑比重,加剧了伊文思蓝的渗漏及毛细血管超微结构的损坏。结论：AQP4基因缺失加剧了脑出血损伤,包括水肿形成、血脑屏障破坏。对脑出血后AQP4表达增高的保护性机制研究可能会为临床治疗脑出血后脑水肿提供新的靶点及思路。

英文摘要：

The purpose of this study was to examine the role of AQP4 in edema formation after intracerebral hemorrhage（ICH） by using AQP4^-/- mice. Methods： ICH was induced by microinjecting 5 μL autologous whole blood into the striatum of AQP4^＋/＋ and AQP4^-/- mice. Neurological deficits, brain edema contents of whole hemorrhagic ipsilateral hemisphere, specific gravity of brain tissue surrounding hematoma, Evans blue leakage and ultrastructure of brain microvessels were compared between AQP4^＋/＋ and AQP4^-/- mice following ICH. Results： Our experiments showed a significant increase of AQP4 expression following ICH in AQP4^＋/＋ mice. AQP4 deletion aggravated neurological deficits and brain edema contents of whole hemorrhagic ipsilateral hemisphere. Besides, it also reduced the specific gravity of brain tissue surrounding hematoma. Moreover, it enhanced Evans blue leakage and ultrastructure of brain microvessel damage. Conclusion： These results suggest that AQP4 deletion increases ICH damage, including edema formation, blood-brain barrier damage. Further studies on the protective role of activated AQP4 expression following ICH may provide useful therapeutic target for ICH-induced brain injury.