Fluoxetine is Neuroprotective in Early Brain Injury via its Antiinflammatory and Anti-apoptotic Effects in a Rat Experimental Subarachnoid Hemorrhage Model
Fluoxetine is Neuroprotective in Early Brain Injury via its Antiinflammatory and Anti-apoptotic Effects in a Rat Experimental Subarachnoid Hemorrhage Model作者机构:Department of Spine Surgery Honghui Hospital Xi'an Jiaotong University College of Medicine Key Laboratory of Resource Biology and Biotechnology in Western China (Ministry of Education) Northwest University
出 版 物:《Neuroscience Bulletin》 (神经科学通报(英文版))
年 卷 期:2018年第34卷第6期
页 面:951-962页
核心收录:
学科分类:10[医学]
基 金:supported by the National Natural Science Foundation of China (81601938) the Natural Science Fund of Shaanxi Province (2016JQ8010) the Science and Technology Projects Fund of Xi’an city (2016050SF/YX06(6))
主 题:Subarachnoid hemorrhage Fluoxetine Blood-brain barrier Microglial activation Neuronal apoptosis
摘 要:Fluoxetine, an anti-depressant drug, has recently been shown to provide neuroprotection in central nervous system injury, but its roles in subarachnoid hemorrhage(SAH) remain unclear. In this study, we aimed to evaluate whether fluoxetine attenuates early brain injury(EBI) after SAH. We demonstrated that intraperitoneal injection of fluoxetine(10 mg/kg per day) significantly attenuated brain edema and blood-brain barrier(BBB) disruption, microglial activation, and neuronal apoptosis in EBI after experimental SAH, as evidenced by the reduction of brain water content and Evans blue dye extravasation, prevention of disruption of the tight junction proteins zonula occludens-1, claudin-5, and occludin, a decrease of cells staining positive for Iba-1, ED-1, and TUNEL and a decline in IL-1 b, IL-6, TNF-a, MDA, 3-nitrotyrosine, and 8-OHDG levels. Moreover, fluoxetine significantly improved the neurological deficits of EBI and long-term sensorimotor behavioral deficits following SAH in a rat model. These results indicated that fluoxetine has a neuroprotective effect after experimental SAH.