神经炎症
氟伏沙明
创伤性脑损伤
神经保护
小胶质细胞
医学
药理学
渗透(HVAC)
中枢神经系统
炎症
免疫学
血清素
内科学
精神科
受体
氟西汀
物理
热力学
作者
Mingming Shi,Liang Mi,Fanjian Li,Ying Liu,Yuan Zhou,Fanglian Chen,Liang Liu,Yan Chai,Weidong Yang,Jianning Zhang,Xin Chen
标识
DOI:10.1089/neu.2021.0355
摘要
Neuroinflammation is an important mediator of secondary injury pathogenesis that exerts dual beneficial and detrimental effects on pathophysiology of the central nervous system (CNS) after traumatic brain injury (TBI). Fluvoxamine is a serotonin selective reuptake inhibitor (SSRI) and has been reported to have the anti-inflammatory properties. However, the mechanisms and therapeutic effects of fluvoxamine in neuroinflammation after TBI have not be defined. In this study, we showed that fluvoxamine inhibited peripheral immune cell infiltration and glia activation at 3 days in mice subjected to TBI. Fluvoxamine treatment promoted microglial/macrophage phenotypic transformation from pro-inflammatory M1-phenotype to anti-inflammatory M2-phenotype in in vivo and in vitro experiments. In addition, fluvoxamine treatment attenuated neuronal apoptosis, blood-brain barrier (BBB) disruption, cerebrovascular damage, and post-traumatic edema formation, thereby improving neurological function of mice subjected to TBI. These findings support the clinical evaluation of fluvoxamine as a neuroprotective therapy for TBI.
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