Wu He, Zhao Ruibo, Qi Jiping, Cong Yuwei, Wang Dandan, Liu Tao, Gu Yunhe, Ban Xiang, Huang Qi
Department of Pathology, First Clinical Hospital, Harbin Medical University, Harbin 150001, People's Republic of China.
J Neurol Sci. 2008 Jul 15;270(1-2):172-83. doi: 10.1016/j.jns.2008.03.010. Epub 2008 Apr 28.
Brain edema is one of the most frequent and serious complications of intracerebral hemorrhage (ICH), but how the ICH cause brain edema is unknown. Our studies were designed to investigate the regulation and distribution of protease nexin-1 (PN-1), thrombin and aquaporin-4 (AQP-4) in brain edema after ICH in rat and human brain in vivo. Our result showed that the severity of cerebral edema resulted from an acute stage of ICH. The PN-1-thrombin system modulated cerebral edema after ICH. Thrombin and AQP-4 increased to aggregate cerebral edema after ICH. In order to control the deleterious effect of thrombin's overexpression, PN-1 appeared quickly and abundantly to inhibit thrombin and lessen the cerebral edema. PN-1 was distributed in neurons and glial cells of cerebral cortex, hippocampus, thalamencephalon, basal ganglia, cerebellum and circum-encephalocoele in rat and human brain. The expression of AQP-4 is different between human and rat. Thus, we demonstrated that the animal experimental approach was, however, not sufficient by itself and needed to be corroborated by observations on human brains.
脑水肿是脑出血（ICH）最常见且严重的并发症之一，但脑出血如何引发脑水肿尚不清楚。我们的研究旨在探讨蛋白酶连接素-1（PN-1）、凝血酶和水通道蛋白-4（AQP-4）在大鼠脑出血及人脑活体脑水肿中的调控及分布情况。我们的结果表明，脑水肿的严重程度源于脑出血的急性期。PN-1-凝血酶系统在脑出血后调节脑水肿。脑出血后，凝血酶和AQP-4增加，加剧脑水肿。为控制凝血酶过度表达的有害作用，PN-1迅速大量出现以抑制凝血酶并减轻脑水肿。PN-1分布于大鼠和人脑的大脑皮质、海马、丘脑、基底神经节、小脑和脑膨出周围的神经元和神经胶质细胞中。AQP-4在人和大鼠中的表达有所不同。因此，我们证明仅靠动物实验方法是不够的，还需要通过对人脑的观察来证实。
