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.

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。}