Neuroprotective Properties of Rutin Hydrate against Scopolamine-Induced Deficits in BDNF/TrkB/ERK/CREB/Bcl2 Pathways.

IF 3.2 Q2 CLINICAL NEUROLOGY
Inturu Sreelatha, Ga-Young Choi, In-Seo Lee, Omkaram Inturu, Hyun-Sook Lee, Yea-Na Park, Cheol-Won Lee, Inkyou Yang, Sungho Maeng, Ji-Ho Park
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Abstract

Background/Objectives: Alzheimer's disease (AD) is an age-related degenerative brain disorder characterized by a progressive decline in cognitive function and memory. This study aimed to evaluate whether rutin hydrate (RH) has neuroprotective effects in an AD-like learning and memory impairment rat model induced by scopolamine (SCO). Methods: The rats were administered with RH (100 mg/kg) and SCO (1.5 mg/kg) and underwent behavioral tests, including the Morris water maze test, Y-maze test, and passive avoidance test, to evaluate their learning and memory abilities. Additionally, long-term potentiation (LTP) was induced to observe changes in the field excitatory postsynaptic potential (fEPSP) activity. Results: RH treatment attenuated the SCO-induced shortening of step-through latency in the passive avoidance (PA) test, increased the percentage of alternation in the Y-maze, and increased the time spent in the target zone in the Morris water maze (MWM). Moreover, RH increased the total activity of fEPSP following theta burst stimulation and attenuated the SCO-induced blockade of fEPSP. RH also ameliorated the SCO-induced decrease in the expression levels of the BDNF, TrkB, ERK, CREB, and Bcl-2 proteins and the increase in the Bax protein level in the rat hippocampus. This demonstrates that RH has beneficial neuroprotective effects in the brain, improving learning, memory, and synaptic plasticity in rats. Conclusions: Our results highlight the molecular and cellular mechanisms through which RH exerts its neuroprotective effects in the prevention and treatment of learning and memory deficit disorders. RH could potentially be used as a therapeutic strategy for the restoration of learning and memory function and the prevention of the progression of AD.

芦丁水合物对东莨菪碱诱导的 BDNF/TrkB/ERK/CREB/Bcl2 通路缺陷的神经保护特性
背景/目标:阿尔茨海默病(AD)是一种与年龄相关的退行性脑部疾病,其特征是认知功能和记忆力逐渐下降。本研究旨在评估芦丁水合物(RH)在东莨菪碱(SCO)诱导的类似 AD 的学习和记忆损伤大鼠模型中是否具有神经保护作用。研究方法给大鼠注射水合芦丁(100 mg/kg)和东莨菪碱(1.5 mg/kg),并进行行为测试,包括莫里斯水迷宫测试、Y-迷宫测试和被动回避测试,以评估其学习和记忆能力。此外,还诱导了长期电位(LTP)以观察场兴奋突触后电位(fEPSP)活性的变化。结果RH治疗减轻了SCO诱导的被动回避(PA)测试中步进潜伏期的缩短,增加了Y迷宫中交替的百分比,并增加了莫里斯水迷宫(MWM)中目标区的停留时间。此外,RH还能提高θ脉冲刺激后fEPSP的总活性,并减轻SCO引起的fEPSP阻滞。RH 还能改善 SCO 引起的大鼠海马中 BDNF、TrkB、ERK、CREB 和 Bcl-2 蛋白表达水平的降低以及 Bax 蛋白水平的升高。这表明 RH 对大脑神经有保护作用,能改善大鼠的学习、记忆和突触可塑性。结论:我们的研究结果凸显了 RH 在预防和治疗学习与记忆障碍方面发挥神经保护作用的分子和细胞机制。RH 有可能被用作恢复学习和记忆功能以及预防注意力缺失症进展的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Neurology International
Neurology International CLINICAL NEUROLOGY-
CiteScore
3.70
自引率
3.30%
发文量
69
审稿时长
11 weeks
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