Role of Protease-Activated Receptor on Brain Injury.

脑损伤和脑肿瘤导致脑水肿。脑水肿是一种病理性的积水在受损的脑组织。预防脑水肿是对大脑的保护。凝血酶和水通道蛋白可能参与脑水肿的病理生理过程。水通道蛋白。凝血酶通过蛋白酶激活受体2具有细胞外蛋白水解和细胞介导的功能。采用脑损伤模型和体外细胞培养模型，分析了蛋白酶激活受体2和水通道蛋白在脑水肿中的作用。采用实时RT-PCR定量评价蛋白酶激活受体2和水通道蛋白的mrna。蛋白酶激活受体2在脑水肿中的作用尚不明确。另一方面，我们发现水通道蛋白在脑水肿中有明确的作用。缺血或挫伤后损伤脑组织渗透压升高。我们的研究表明，损伤脑组织中渗透压的增加会触发星形胶质细胞中水通道蛋白的过度表达。在高渗透压刺激后，低温抑制培养的星形细胞水通道蛋白的过度表达。根据渗透梯度，水分子容易通过过度表达的水通道向损伤组织移动。低温抑制星形细胞水通道蛋白的过度表达。这种抑制可能有利于脑损伤，防止脑水肿。

Brain injury and brain tumor causes brain edema. Brain edema is a pathological water accumulation in injured brain tissues. Prevention of the brain edema leads to the brain protection. A protease THROMBIN and a water channel protein AQUAPORIN may contribute the pathophysiology of the brain edema. aquaporin. Thrombin has both extracellular proteolysis and cell mediated functions thorough the protease-activated receptor 2.We analyzed the roles of protease-activated receptor 2 and aquaporin on the brain edema using in vivo model of brain injury and in vitro model of cell cultures. Using real-time RT-PCR, we quantitatively evaluated mRNAs of protease-activated receptor 2 and aquaporin.We could not find the definitive roles of protease-activated receptor 2 on the brain edema. On the other hand, we found a clear role of aquaporin on the brain edema. Osmolarity of injured brain tissues increased after ischemia or contusion. Our study suggests that an increase of osmolarity in injured brain tissues triggers overexpression of aquaporin in astrocytes. Hypothermia inhibits this overexpression of cultured astrocytic aquaporin after the hyper osmolar stimulation.According to the osmotic gradient, water molecules easily move to the injured tissues through the water channels aquaporin that are excessively expressed. Hypothermia inhibits this overexpression of astrocytic aquaporin. This inhibition may be benefit for the injured brain to prevent the brain edema.