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目的:研究大鼠脑缺血后水通道蛋白4(AQP4)在脑内的表达及N-甲基-D-天冬氨基酸(NMDA)受体拮抗剂艾芬地尔对其的调节作用。方法:线栓法制作大脑中动脉阻塞(middle cerebra lartery occlusion,MACO)局灶性脑缺血模型;干湿重法测量脑组织含水量以评估脑水肿的程度;免疫组化,免疫蛋白印记法测量AQP4(水通道蛋白4)的表达。结果:与假手术组比较,模型组和艾芬地尔组脑组织含水量、梗死灶周围AQP4表达明显增加;与模型组比较,艾芬地尔组能显著减少脑组织含水量,减轻梗死灶周围AQP4表达,差异有统计学意义。结论:缺血损伤后脑组织的AQP4表达上升,脑水肿明显,给予艾芬地尔后可抑制AQP4的表达,减轻脑水肿。
AIM: To investigate the expression of aquaporin-4 (AQP4) in rat brain and the effect of iFedipine, an N-methyl-D-aspartate amino acid (NMDA) receptor antagonist, on it. Methods: The focal cerebral ischemia model of middle cerebral artery occlusion (MACO) was made by the method of thread embolism. The degree of cerebral edema was measured by the wet-dry weight method. The degree of brain edema was evaluated by immunohistochemistry and immunocytochemistry AQP4 (Aquaporin 4) expression was measured. Results: Compared with the sham-operation group, the water content of brain tissue and the expression of AQP4 around the infarct area in the model group and the isofenzil group were significantly increased. Compared with the model group, the group of isoproterenol significantly reduced the water content in the brain tissue and reduced the infarct size Surrounding AQP4 expression, the difference was statistically significant. Conclusion: The expression of AQP4 in brain tissue after cerebral ischemic injury is increased and brain edema is obvious. After given isoferil, it can inhibit the expression of AQP4 and relieve cerebral edema.