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σ1a adaptin regulates APP transgolgi sorting in neurons

机译:σ1aAdaptin调节神经元中的APP transgolgi分类

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Vagus nerve stimulation attenuates glial-mediated inflammation in the poly-I:C-induced fatigue in rats The over-activation of immune system results in fatigue and decrease physical activity in animal model and human. Viral infec- tion in central nervous system triggers astrogliosis and microgliosis accompanied by enhanced production of pro-inflammatory cytokines such as interleukin-1b (IL-1b), interleukin 6 (IL-6) and tumor necrosis factor-a (TNF-a). Polyinosinic-polycytidylic acid (poly-I:C), virus-mimicking synthetic double-stranded RNA, is a ligand of toll-like receptor-3 (TLR3) and is able to initiate rapid innate immune responses. It was previously reported that poly-I:C-induced rat showed glial activation in brain resulted in decreased spontaneous running wheel and locomotor activity and impaired learning and memory. Vagus nerve stimulation (VNS) has been explored in multiple experimental animal models and clinical trials of epileptic seizure and drug-resistant depres- sion. Especially, anti-inflammatory properties of VNS have been reported in chemical-induced animal models such as lipopolysac- charide (LPS), an endotoxin derived from Gram-negative bacteria.
机译:迷走神经刺激减轻了多聚I:C诱导的大鼠疲劳中的神经胶质介导的炎症。免疫系统的过度激活导致疲劳,并降低了动物模型和人类的身体活动。中枢神经系统中的病毒感染会引发星形胶质细胞增生和小胶质细胞增生,并伴有促炎细胞因子如白介素-1b(IL-1b),白介素6(IL-6)和肿瘤坏死因子-a(TNF-a)的产生。 。模仿病毒的合成双链RNA聚肌苷酸-聚胞苷酸(poly-I:C)是toll-like receptor-3(TLR3)的配体,能够启动快速的先天免疫应答。以前有报道说,聚-I:C诱导的大鼠大脑中的神经胶质细胞活化,导致自发行走轮和运动能力降低,并损害学习和记忆。迷走神经刺激(VNS)已经在多种实验动物模型以及癫痫发作和耐药性抑郁症的临床试验中得到了探索。尤其是,在化学诱导的动物模型中,例如脂多糖(LPS),即革兰氏阴性细菌衍生的内毒素,已经报道了VNS的抗炎特性。

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