促炎细胞因子
神经炎症
突触蛋白I
海马体
下调和上调
神经保护
免疫印迹
肿瘤坏死因子α
小RNA
内科学
医学
心理学
炎症
神经科学
生物
生物化学
小泡
膜
基因
突触小泡
遗传学
作者
Yao Chen,Qi An,Shuting Yang,Yu-Lu Chen,Lei Tong,Li-Li Ji
标识
DOI:10.1016/j.expneurol.2022.114154
摘要
Abstract BackgroundMicroRNA-124-3p (miR-124) plays an important role in neuroprotective functions in various neurological disorders, but whether miR-124 participates in the pathological progression of posttraumatic stress disorder (PTSD) remains poorly understood. MethodsIn the present study, we evaluated the level of neuroinflammation in the hippocampus of rats exposed to single-prolonged stress (SPS) by western blot and immunofluorescence staining, while the effect of miR-124 on PTSD-like behaviors was evaluated by behavioral test. ResultsOur results demonstrated that the level of miR-124 in the hippocampus of rats exposed to SPS was downregulated and that the upregulation of miR-124 could alleviate the PTSD-like behaviors of SPS rats. This effect of miR-124 might be achieved through TNF receptor-associated Factor 6 (TRAF6), which is a target gene of miR-124 and plays an important role in the immune and inflammatory reaction by regulating nuclear factor kappa-B (NF-κB). Furthermore, we found that miR-124 not only decreased the level of proinflammatory cytokines but also increased the expression levels of synaptic proteins (PSD95 and synapsin I) and regulated the morphology of neurons. ConclusionThese results suggested that miR-124 might attenuate PTSD-like behaviors and decrease the level of proinflammatory cytokines by downregulating the expression of TRAF6 in the hippocampus of rats exposed to SPS.
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