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Nutritional supplementation of gallic acid ameliorates Alzheimer-type hippocampal neurodegeneration and cognitive impairment induced by aluminum chloride exposure in adult Wistar rats
Drug and Chemical Toxicology ( IF 2.1 ) Pub Date : 2020-04-24 , DOI: 10.1080/01480545.2020.1754849
B Ogunlade 1 , S A Adelakun 1 , J A Agie 1
Affiliation  

Abstract

Prolonged exposure to aluminum through occupational hazards or food/water intake has been linked to the occurrence of Alzheimer’s disease (AD). This study aimed at investigating the neuroprotective effects of Gallic Acid (GA) against aluminum-chloride induced AD in adult Wistar rats. Twenty eight (28) adult Wistar rats were divided into four groups (n = 7). Group A received normal saline as placebo; Group B received 200 mg/kg bw of AlCl3 only; Group C received 100 mg/kg bw of GA only and group D received 100 mg/kg bw of GA and 200 mg/kg bw of AlCl3. At the end of the 60 days experiment, blood samples were collected to obtain serum for analysis and the brain was harvested. Neurobehavioural tests (Morris Water maze, Y-Maze), neurotransmitter levels, oxidative stress markers, serum electrolytes, antioxidant enzymes and histological assessment were carried out. There was a significant decrease in antioxidant enzymes (CAT, GSH and SOD), serum electrolyte (except K+) and neurotransmitter levels (except norepinephrine) with corresponding increase in stress markers (MDA, H2O2 and NO) among group B compared to control but was restored nearly to normal after GA administration. Neurobehavioral tests showed decreased spatial memory impairment and learning deficit in group B compared to control but was ameliorated with GA administration. Histological observation showed neurofibrillary tangles and amyloid plaques in the external granular layer of group B but protected by GA administration. Nutritional supplementation of GA preserve the morphological and physiological integrity of the hippocampus against environmental neurotoxins (AlCl3) by mopping up free radicals associated with oxidative stress induced AD.



中文翻译:

没食子酸的营养补充可改善成年 Wistar 大鼠氯化铝暴露引起的阿尔茨海默型海马神经变性和认知障碍

摘要

通过职业危害或食物/水摄入而长期接触铝与阿尔茨海默病 (AD) 的发生有关。本研究旨在研究没食子酸 (GA) 对成年 Wistar 大鼠氯化铝诱导的 AD 的神经保护作用。二十八 (28) 只成年 Wistar 大鼠分为四组 ( n  = 7)。A组接受生理盐水作为安慰剂;B 组仅接受 200 mg/kg bw 的 AlCl 3;C 组仅接受 100 mg/kg bw 的 GA,D 组接受 100 mg/kg bw 的 GA 和 200 mg/kg bw 的 AlCl 3. 在 60 天的实验结束时,采集血样以获得血清进行分析,并收获大脑。进行了神经行为测试(Morris Water maze、Y-Maze)、神经递质水平、氧化应激标志物、血清电解质、抗氧化酶和组织学评估。抗氧化酶(CAT、GSH 和 SOD)、血清电解质(K+ 除外)和神经递质水平(去甲肾上腺素除外)显着降低,而应激标志物(MDA、H 2 O 2相应增加)和 NO)在 B 组中与对照组相比,但在 GA 给药后几乎恢复正常。神经行为测试显示,与对照组相比,B 组的空间记忆障碍和学习缺陷减少,但使用 GA 后得到改善。组织学观察显示B组外颗粒层有神经原纤维缠结和淀粉样斑块,但受到GA保护。GA 的营养补充通过清除与氧化应激诱导的 AD 相关的自由基来保持海马体对环境神经毒素 (AlCl 3 ) 的形态和生理完整性。

更新日期:2020-04-24
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