NK3 受体信号在躁郁症中的新作用

Wei Zhang, Linyao Yu, Yaoqin Shi, Yingtian Zhang, Min Xu, Yang Xu, Chunmei Li, Jingwei Tian
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摘要

目的:躁郁症(BD)影响着全球 1%以上的人口,但治疗方法却很有限。神经激肽B(NKB)-神经激肽B受体(NK3R)参与多种情绪活动。本研究探讨了NK3受体信号传导在躁狂症中的作用:本研究采用脑室内给药 OUA 诱导的躁狂症模型,探讨 NK3R 信号在躁狂症中的可能作用。通过在海马中使用 shRNA 基因敲除编码 NK3R 的 TACR3 基因,并全身给药 NK3R 拮抗剂 ESN364,评估了 NK3R 在 OUA 诱导的 BD 表达中的参与。采用生化技术检测 BD 大鼠海马中与 NK3R 相关的信号变化和氧化应激参数:结果:NK3R在BD大鼠海马中的表达水平升高。结果:NK3R在BD大鼠海马中的表达水平升高,敲除海马中的TACR3和ESN364治疗均可逆转BD大鼠的躁狂样和抑郁样行为:这些结果表明,NK3R 信号在 BD 发病机制中起着关键作用,ESN364 等 NK3R 药物拮抗剂可能是治疗 BD 的一种新策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A novel role of NK3 receptor signaling in bipolar disorder
Objective: Bipolar disorder (BD) affects more than 1% of the global population with limited therapeutic options. The neurokinin B (NKB)-neurokinin B receptor (NK3R) is involved in a variety of emotional activities. This study explored the role of NK3 receptor signaling in bipolar disorder.Materials and methods: In this study, a model of intracerebroventricular (ICV) administration of OUA-induced BD was used to investigate the possible role of NK3R signaling in BD. The involvement of NK3R in the expression of OUA-induced BD was assessed by genetically knocking down the NK3R-encoding TACR3 gene with shRNA approach in the hippocampus and systemic administration of a NK3R antagonist ESN364,. Biochemical techniques were used to examine the NK3R-associated signaling changes and the oxidative stress parameters in the hippocampus of BD rats.Result: The NK3R expression level was elevated in the hippocampus BD rats. Both TACR3 knockdown in the hippocampus and ESN364 treatment reversed the manic-like and depression-like behaviors in BD rats Inhibition of the NK3R signaling reversed oxidative stress-induced damage via upregulating the BDNF signaling pathway in the hippocampus.Conclusion: These results demonstrated that NK3R signaling plays a key role in the pathogenesis of BD and that pharmacological antagonist of NK3R such as ESN364 could represent a novel therapeutic strategy for the management of BD.
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