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司来吉兰对抗淀粉样蛋白β诱导的焦虑样行为和记忆损伤的保护作用。

Protective effects of selegiline against amyloid beta-induced anxiety-like behavior and memory impairment.

机构信息

Department of Biology, Faculty of Basic Science, Bu-Ali Sina University, Hamedan, Iran.

Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.

出版信息

Brain Behav. 2024 Jun;14(6):e3599. doi: 10.1002/brb3.3599.

DOI:10.1002/brb3.3599
PMID:38873869
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11176901/
Abstract

BACKGROUND

Alzheimer's disease (AD) is a complex and common neurodegenerative disorder. The present study aimed to investigate the potential effects of selegiline (SEL) on various aspects of memory performance, anxiety, and oxidative stress in an AD rat model induced by intracerebroventricular injection of amyloid beta (Aβ).

METHODS

Oral administration of SEL at a dose of 0.5 mg/kg/day was performed for 30 consecutive days. Following the 30 days, several tests, including the open-field, elevated plus-maze, novel object recognition, Morris water maze, and passive avoidance learning were conducted to assess locomotor activity, anxiety-like behavior, recognition memory, spatial memory, and passive avoidance memory, respectively.

RESULTS

The results indicate that the induction of AD in rats led to recognition memory, spatial memory, and passive avoidance memory impairments, as well as increased anxiety. Additionally, the AD rats exhibited a decrease in total antioxidant capacity and an increase in total oxidant status levels, suggesting an imbalance in oxidative-antioxidant status. However, the administration of SEL improved memory performance, reduced anxiety, and modulated oxidative-antioxidant status in AD rats.

CONCLUSIONS

These findings provide evidence that SEL may alleviate anxiety-like behavior and cognitive deficits induced by Aβ through modulation of oxidative-antioxidant status.

摘要

背景

阿尔茨海默病(AD)是一种复杂且常见的神经退行性疾病。本研究旨在探讨司来吉兰(SEL)对脑室内注射淀粉样蛋白β(Aβ)诱导的 AD 大鼠模型在记忆表现、焦虑和氧化应激各方面的潜在影响。

方法

连续 30 天给予 SEL 口服剂量为 0.5mg/kg/天。30 天后,通过旷场实验、高架十字迷宫实验、新物体识别实验、Morris 水迷宫实验和被动回避学习实验,分别评估运动活动、焦虑样行为、识别记忆、空间记忆和被动回避记忆。

结果

结果表明,AD 大鼠的诱导导致了识别记忆、空间记忆和被动回避记忆损伤,以及焦虑增加。此外,AD 大鼠的总抗氧化能力降低,总氧化状态水平升高,表明氧化-抗氧化状态失衡。然而,SEL 的给药改善了 AD 大鼠的记忆表现,减轻了焦虑,并调节了氧化-抗氧化状态。

结论

这些发现提供了证据表明,SEL 可能通过调节氧化-抗氧化状态来减轻 Aβ诱导的焦虑样行为和认知缺陷。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5307/11176901/9a0b16a10e46/BRB3-14-e3599-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5307/11176901/c4a1017b6b24/BRB3-14-e3599-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5307/11176901/86afca93319d/BRB3-14-e3599-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5307/11176901/842dd7e90217/BRB3-14-e3599-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5307/11176901/c88c5cc31dc4/BRB3-14-e3599-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5307/11176901/288573dcda4c/BRB3-14-e3599-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5307/11176901/9a0b16a10e46/BRB3-14-e3599-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5307/11176901/c4a1017b6b24/BRB3-14-e3599-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5307/11176901/86afca93319d/BRB3-14-e3599-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5307/11176901/842dd7e90217/BRB3-14-e3599-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5307/11176901/c88c5cc31dc4/BRB3-14-e3599-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5307/11176901/288573dcda4c/BRB3-14-e3599-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5307/11176901/9a0b16a10e46/BRB3-14-e3599-g006.jpg

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