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首页> 外文期刊>Biochemical and Biophysical Research Communications >Intradiencephalon injection of histamine inhibited the recovery of locomotor function of spinal cord injured zebrafish
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Intradiencephalon injection of histamine inhibited the recovery of locomotor function of spinal cord injured zebrafish

机译:Intrationalyphalon注射组胺的抑制脊髓受伤斑马鱼的运动功能的回收

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摘要

Human spinal cord injury (SCI) usually causes irreversible disability beneath the injured site due to poor neural regeneration. On the contrary, zebrafish show significant regenerative ability after SO, thus is usually worked as an animal model for studying neuroregeneration. Most of the previous SCI studies focused on the local site of SCI, the supraspinal-derived signals were rarely mentioned. Here we showed that intradiencephalon injection of histamine (HA) inhibited the locomotor recovery in adult zebrafish post-SCI. Immunofluorescence results showed that intradiencephalon HA administration increased the activated microglia 3 days post injury (dpi), promoted the proliferation of radial glial cells at 7 dpi and affected the morphology of radial glial cells at 11 dpi. Furthermore, quantitative real-time polymerase chain reaction (qRT-PCR) results showed that intradiencephalon HA administration also reduced the expression of neurotrophic factors including brain-derived neurotrophic factor (BDNF) and insulin-like growth factorl (IGF-1) at the lesion site, however, had no effect on the expression of pro inflammatory factors such as TNF-alpha and IL-1 beta. Hence, our data suggested that exogenous intradiencephalon HA retarded locomotor recovery in spinal cord injured zebrafish via modulating the repair microenvironment. (C) 2017 Elsevier Inc. All rights reserved.
机译:由于神经再生不良,人脊髓损伤(SCI)通常会导致受伤部位下的不可逆性残疾。相反,斑马鱼在此后显示出显着的再生能力,因此通常作为学习神经循环的动物模型。最先前的SCI研究集中于SCI的局部位点,很少提及求求衍生的信号。在这里,我们表明,Intrancephalon注入组胺(HA)抑制了成年斑马鱼后SCI中的运动恢复。免疫荧光结果表明,Intrationealphalon HA给药在损伤后3天增加了活化的小胶质细胞(DPI),促进了7 DPI的桡骨胶质细胞的增殖,并影响了11 dpi的桡骨神经胶质细胞的形态。此外,定量实时聚合酶链反应(QRT-PCR)结果表明,Intrancealphalon HA给药还降低了神经营养因子的表达,包括脑衍生的神经营养因子(BDNF)和病变处的胰岛素样生长因子(IGF-1)然而,遗址对TNF-α和IL-1β等促炎因子的表达没有影响。因此,我们的数据表明,通过调节修复微环境,外源性Intrationealphalon Ha延迟在脊髓受伤的斑马鱼中恢复。 (c)2017年Elsevier Inc.保留所有权利。

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