阿米替林激活TrkA帮助神经元增长和减弱Anesthesia-Induced神经退化的大鼠背根神经节神经元。

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郑X,陈F,郑T,黄F,陈J,你W

阿米替林激活TrkA帮助神经元增长和减弱Anesthesia-Induced神经退化的大鼠背根神经节神经元。

医学(巴尔的摩)。95年5月,2016年(18):e3559。doi: 10.1097 / MD.0000000000003559。

PubMed ID

27149473 (在PubMed

]

文摘

三环抗抑郁药阿米替林(AM)已被证明对神经元产生神经营养活性。我们因此探索是否可能援助的神经发展和保护anesthesia-induced neuro-injury年轻脊髓背根神经节(DRG)神经元。从已经大鼠DRG外植体的准备。协助诊断相关神经发展的影响是通过免疫组织化学方法检测方式存在剂量依赖的相关性。AM-induced基因和蛋白质表达的变化,以及磷酸化的酪氨酸激酶受体A (TrkA)和B (TrkB)在打钻,检查了定量实时聚合酶链反应和免疫印迹。背根神经节神经退化的影响是在衰减lidocaine-induced被免疫组织化学检查,和小干扰RNA (siRNA)介导TrkA / B下调。阿米替林stimulated DRG neuronal development in dose-dependent manner, but exerted toxic effect at concentrations higher than 10 M. AM activated TrkA in DRG through phosphorylation, whereas it had little effect on TrkB-signaling pathway. AM reduced lidocaine-induced DRG neurodegeneration by regenerating neurites and growth cones. Moreover, the neuroprotection of AM on lidocaine-injured neurodegeneration was blocked by siRNA-mediated TrkA down-regulation, but not by TrkB down-regulation.Amitriptyline facilitated neuronal development and had protective effect on lidocaine-induced neurodegeneration, very likely through the activation of TrkA-signaling pathway in DRG.

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药物靶点

药物	目标	类	生物	药理作用	行动
阿米替林	神经生长因子受体高亲和力	蛋白质	人类	未知的	受体激动剂 激活剂	细节