Methylene Blue Attenuates Impaired Cognitive Functions and Reduces Hippocampal Aβ Levels and Oxidative Stress in D-Galactose-Induced Alzheimer’s Disease Mouse Model

IF 0.5 4区 生物学 Q4 BIOLOGY Biology Bulletin Pub Date : 2024-03-26 DOI:10.1134/s106235902360455x
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Abstract

Methylene blue (MB) has a long story of use and has been employed for various diseases, however, most of its current rekindled research is related to its function in the mitochondria. MB is gaining interest as a possible treatment because mitochondrial dysfunction is an apparent unifying pathogenic characteristic of a variety of neurodegenerative conditions. Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by impairment of cognitive functions. This study aims to investigate whether MB treatment improves impaired cognitive functions and reduces hippocampal amyloid-β levels and oxidative stress in a D-galactose-induced AD mouse model. Twenty-four wild-type Balb/c mice were randomly divided into four groups (control, D-galactose-induced AD, MB-treated AD, and only MB-treated mice). Mice in the corresponding groups were injected with D-galactose (50 mg/kg, s.c.) for 60 days. In the MB treatment groups, the mice were treated with MB (2 mg/kg, orally) for the last 14 days of treatments. The Morris water maze test was used to assess spatial learning and memory functions. Amyloid β-42, malondialdehyde, superoxide dismutase, and nitric oxide levels in the hippocampi of mice were measured using ELISA and spectrophotometry. MB treatment improved impaired learning and memory functions induced by D-galactose administration and decreased amyloid β-42 concentration in the hippocampi of mice. Malondialdehyde level was found to decrease in MB-treated mice compared to D-galactose-induced AD mice in the hippocampus and plasma. The hippocampus of MB-treated mice displayed increased superoxide dismutase activity while decreased nitric oxide concentration compared to the ones of D-galactose-induced AD mice. MB has been shown to improve learning and memory impairments, as well as reduce Aβ-42 concentration and oxidative stress in the hippocampus of D-galactose-induced AD mice. The findings of this study demonstrate that MB may offer potential benefits as a repurposed agent for AD.

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亚甲蓝可减轻认知功能损伤并降低 D-半乳糖诱导的阿尔茨海默病小鼠模型的海马 Aβ 水平和氧化应激
摘要 亚甲蓝(MB)的使用由来已久,曾被用于治疗各种疾病,但目前重新启动的研究大多与亚甲蓝在线粒体中的功能有关。线粒体功能障碍是多种神经退行性疾病的一个明显的统一致病特征,因此甲基溴作为一种可能的治疗方法正受到越来越多的关注。阿尔茨海默病(AD)是一种以认知功能障碍为特征的进行性神经退行性疾病。本研究旨在探讨甲基溴治疗是否能改善认知功能受损,并降低 D-半乳糖诱导的 AD 小鼠模型的海马淀粉样蛋白-β 水平和氧化应激。24 只野生型 Balb/c 小鼠被随机分为四组(对照组、D-半乳糖诱导的 AD 小鼠组、MB 治疗的 AD 小鼠组和仅 MB 治疗的小鼠组)。相应组的小鼠连续 60 天注射 D-半乳糖(50 毫克/千克,静脉注射)。在甲基溴治疗组中,小鼠在治疗的最后 14 天口服甲基溴(2 毫克/千克)。莫里斯水迷宫试验用于评估小鼠的空间学习和记忆功能。使用 ELISA 和分光光度法测量了小鼠海马中淀粉样β-42、丙二醛、超氧化物歧化酶和一氧化氮的水平。甲基溴治疗改善了服用 D-半乳糖引起的学习和记忆功能受损,降低了小鼠海马中淀粉样蛋白 β-42 的浓度。经甲基溴治疗的小鼠海马和血浆中的丙二醛水平比D-半乳糖诱导的AD小鼠低。与 D-半乳糖诱导的 AD 小鼠相比,经甲基溴处理的小鼠海马的超氧化物歧化酶活性增加,而一氧化氮浓度降低。有研究表明,甲基溴可改善学习和记忆障碍,并降低 Aβ-42 浓度和 D-半乳糖诱导的 AD 小鼠海马中的氧化应激。这项研究的结果表明,甲基溴作为一种治疗注意力缺失症的再用途药物可能具有潜在的益处。
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来源期刊
Biology Bulletin
Biology Bulletin 生物-生物学
CiteScore
0.70
自引率
20.00%
发文量
84
审稿时长
4-8 weeks
期刊介绍: Biology Bulletin (Izvestiya Rossiiskoi Akademii Nauk – Seriya Biologicheskaya) is an interdisciplinary journal of general biology. It focuses on fundamental studies in the fields of cell biology, biochemistry, zoology, botany, physiology, and ecology. This journal publishes current materials of experimental studies and surveys on current problems in general biology. It also publishes information on scientific conferences and new books in the fields of general biology.
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