Absence in CX3CR1 receptor signaling promotes post‐ischemic stroke cognitive function recovery through suppressed microglial pyroptosis in mice

莫里斯水上航行任务 CX3CR1型 上睑下垂 神经发生 内斯汀 海马结构 冲程(发动机) 神经科学 海马体 纽恩 受体 基因剔除小鼠 细胞生物学 医学 药理学 病理 神经干细胞 心理学 生物 内科学 免疫组织化学 趋化因子受体 干细胞 趋化因子 工程类 炎症体 机械工程
作者
Yangyang Ge,Juexi Yang,Jiayi Chen,Maosha Dai,Xiaoke Dou,Shanglong Yao,Cong Yao,Yun Lin
出处
期刊:CNS Neuroscience & Therapeutics [Wiley]
卷期号:30 (2) 被引量:2
标识
DOI:10.1111/cns.14551
摘要

Abstract Background Post‐stroke cognitive impairment (PSCI) is a major source of morbidity and mortality after stroke, but the pathological mechanisms remain unclear. Previous studies have demonstrated that the CX3CR1 receptor plays a crucial role in maintaining an early protective microenvironment after stroke, but whether it persistently influences cognitive dysfunction in the chronic phase requires further investigation. Methods Mouse was used to establish a middle cerebral artery occlusion (MCAO)/reperfusion model to study PSCI. Cognitive function was assessed by the Morris water maze (MWM) and the novel object recognition test. Neurogenesis was assessed by immunofluorescence staining with Nestin + /Ki67 + and DCX + /BrdU + double‐positive cells. The cerebral damage was monitored by [ 18 F]‐DPA‐714 positron emission tomography, Nissel, and TTC staining. The pyroptosis was histologically, biochemically, and electron microscopically examined. Results Upon MCAO, at 28 to 35 days, CX3CR1 knockout (CX3CR1 −/− ) mice had better cognitive behavioral performance both in MWM and novel object recognition test than their CX3CR1 +/− counterparts. Upon MCAO, at 7 days, CX3CR1 −/− mice increased the numbers of Nestin + /Ki67 + and DCX + /BrdU + cells, and meanwhile it decreased the protein expression of GSDMD, NLRP3 inflammasome subunit, caspase‐1, mature IL‐1β/IL‐18, and p‐P65 in the hippocampus as compared with CX3CR1 +/− mice. In addition, CX3CR1 −/− mice could reverse infarct volume in the hippocampus region post‐stroke. Conclusion Our study demonstrated that CX3CR1 gene deletion was beneficial to PSCI recovery. The mechanism might lie in inhibited pyroptosis and enhanced neurogenesis. CX3CR1 receptor may serve as a therapeutic target for improving the PSCI.
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