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丁硫氨酸减弱了东莨菪碱诱导的大鼠记忆损伤模型中乙酰胆碱能/BDNF/Caspase-3 通路介导的行为障碍。

Butin attenuates behavioral disorders via cholinergic/BDNF/Caspase-3 pathway in scopolamine-evoked memory deficits in rats.

机构信息

Department of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah, Saudi Arabia.

出版信息

Eur Rev Med Pharmacol Sci. 2024 Feb;28(3):981-994. doi: 10.26355/eurrev_202402_35334.

DOI:10.26355/eurrev_202402_35334
PMID:38375702
Abstract

OBJECTIVE

Recent research suggests that butin may also exert neuroprotective effects. However, its influence on cognitive performance and, specifically, its potential to mitigate scopolamine-induced memory impairment remains unexplored. The aim of the study is to investigate the effects of butin on the cognitive and behavioral performance of rats with scopolamine-induced memory impairment.

MATERIALS AND METHODS

Scopolamine-injected memory-impediment model in rats was used to determine the efficacy of butin in higher and lower doses (10 and 20 mg/kg) for 14 days. Y-maze, along with Morris water, was used to assess the ability to recall spatial and working information. Biochemistry-related functions such as acetylcholinesterase, choline acetyltransferase, superoxide dismutase, glutathione transferase, malonaldehyde, catalase, nitric oxide, and neurotransmitters levels were estimated as indicators of free radical damage. Furthermore, we evaluated neuro-inflammatory responses by assessing tumor necrosis factor-alpha (TNF-α), interleukin 1 beta (IL-1β), interleukin-6 (IL-6), brain-derived neurotrophic factor (BDNF) and caspase-3 immuno-reactive proteins.

RESULTS

When assessed through behavioral paradigms, the butin-treated group enhanced the spatial and working memory of rodents. Scopolamine caused a substantial alteration in biochemical-related parameters, neuronal enzymatic, inflammation responses and apoptosis markers prominently restored by butin.

CONCLUSIONS

This study concludes that butin protects scopolamine-injected rats from behavioral impairments and neuronal damage by reducing apoptosis and neuroinflammation.

摘要

目的

最近的研究表明,丁布还可能发挥神经保护作用。然而,它对认知表现的影响,特别是减轻东莨菪碱引起的记忆障碍的潜力,尚未得到探索。本研究旨在研究丁布对东莨菪碱致记忆障碍大鼠认知和行为表现的影响。

材料和方法

采用东莨菪碱注射致记忆障碍大鼠模型,确定丁布高、低剂量(10 和 20mg/kg)14 天的疗效。Y 迷宫和 Morris 水迷宫用于评估空间和工作信息记忆能力。乙酰胆碱酯酶、胆碱乙酰转移酶、超氧化物歧化酶、谷胱甘肽转移酶、丙二醛、过氧化氢酶、一氧化氮和神经递质水平等与生物化学相关的功能被评估为自由基损伤的指标。此外,我们通过评估肿瘤坏死因子-α(TNF-α)、白细胞介素 1β(IL-1β)、白细胞介素 6(IL-6)、脑源性神经营养因子(BDNF)和半胱天冬酶-3 免疫反应蛋白来评估神经炎症反应。

结果

通过行为范式评估,丁布治疗组增强了啮齿动物的空间和工作记忆。东莨菪碱显著改变了与生物化学相关的参数、神经元酶、炎症反应和凋亡标志物,而丁布明显恢复了这些参数。

结论

本研究得出结论,丁布通过减少凋亡和神经炎症,保护东莨菪碱注射大鼠免受行为障碍和神经元损伤。

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