Alrikabi Afaf, Allahyani Wasayf, Shaghath Amjad, Alrashdi Jawaher, Almoqhem Reem, Alasmari Fawaz, Al-Qerem Walid, Albasher Gadah
Department of Zoology, College of Science, King Saud University, Riyadh, Saudi Arabia.
Department of Biology, College of Science, University of Hail, Hail, Saudi Arabia.
Front Neurosci. 2025 Jul 23;19:1634601. doi: 10.3389/fnins.2025.1634601. eCollection 2025.
Alzheimer's disease (AD) is a devastating neurodegenerative disorder characterized by cognitive decline and neuronal damage. Cadmium exposure has been implicated in AD pathogenesis. This study aimed to investigate the potential therapeutic effects of Ebixa (memantine), , and selenium in a cadmium-induced rat model of AD. Adult male Wistar rats were divided into six groups: control, control + Ginkgo-treated, cadmium chloride (CdCl2), CdCl2 + Ebixa-treated, CdCl2 + Ginkgo, and CdCl2 + Ginkgo + Selenium. Behavioral tests, including the Morris water maze and passive avoidance learning, were conducted. Additionally, biochemical analysis of acetylcholine (Ach), choline acetyltransferase (AchT), and acetylcholinesterase (AChE) levels in brain homogenates was performed. Histological sections of the cerebral cortex, cerebellum, and medulla were examined. Apoptotic assessment was conducted using the TUNEL assay. CdCl2 exposure resulted in cognitive deficits, reduced Ach levels, and neuronal damage, mirroring AD-like characteristics. Ebixa treatment improved spatial memory behavior as well as Ach, AchT and AChE levels in the brain. and selenium co-administration increased the number of crossings in the Morris water maze test, suggesting memory preservation. Additionally, exhibited potential cholinergic system protective effects. Histological analysis revealed neuroprotection in the cerebral cortex, cerebellum, and medulla. TUNEL assays demonstrated anti-apoptotic effects of both Ebixa and the combination of Ginkgo and selenium. Ebixa, , and selenium showed promise in mitigating cognitive deficits and preserving neuronal structures in a CdCl2-induced AD manifestation in rats. These findings provide insights into potential therapeutic strategies for AD and warrant further investigation.
阿尔茨海默病（AD）是一种具有毁灭性的神经退行性疾病，其特征为认知功能衰退和神经元损伤。镉暴露与AD的发病机制有关。本研究旨在探讨易倍申（美金刚）、银杏叶提取物以及硒在镉诱导的大鼠AD模型中的潜在治疗作用。成年雄性Wistar大鼠被分为六组：对照组、对照组 + 银杏叶提取物处理组、氯化镉（CdCl2）组、CdCl2 + 易倍申处理组、CdCl2 + 银杏叶提取物组以及CdCl2 + 银杏叶提取物 + 硒组。进行了包括莫里斯水迷宫和被动回避学习在内的行为测试。此外，还对脑匀浆中乙酰胆碱（Ach）、胆碱乙酰转移酶（AchT）和乙酰胆碱酯酶（AChE）水平进行了生化分析。检查了大脑皮层、小脑和延髓的组织学切片。使用TUNEL法进行凋亡评估。CdCl2暴露导致认知缺陷、Ach水平降低和神经元损伤，呈现出类似AD的特征。易倍申治疗改善了空间记忆行为以及大脑中的Ach、AchT和AChE水平。银杏叶提取物和硒联合给药增加了莫里斯水迷宫测试中的穿越次数，表明记忆得到了保留。此外，银杏叶提取物显示出潜在的胆碱能系统保护作用。组织学分析显示大脑皮层、小脑和延髓有神经保护作用。TUNEL分析表明易倍申以及银杏叶提取物和硒的组合具有抗凋亡作用。易倍申、银杏叶提取物和硒在减轻镉诱导的大鼠AD表现中的认知缺陷和保留神经元结构方面显示出前景。这些发现为AD的潜在治疗策略提供了见解，值得进一步研究。
