Apigenin mitigates oxidative stress, neuroinflammation, and cognitive impairment but enhances learning and memory in aluminum chloride-induced neurotoxicity in rats

IF 13 1区医学 Q1 CLINICAL NEUROLOGY

Alzheimer's & Dementia Pub Date : 2025-05-02 DOI:10.1002/alz.70223

Ademola Adetokunbo Oyagbemi, Omowumi Moromoke Femi-Akinlosotu, Adedunsola Adewunmi Obasa, Moses Semilore Ojo, Adeola Temitope Salami, Temitayo Olabisi Ajibade, Charles Etang Onukak, Olumayowa Olawumi Igado, Oluwaseun Olarenwaju Esan, Taiwo Olaide Oyagbemi, Adewumi Victoria Adeogun, Omolola Victoria Awoyomi, Joseph E. Ikokide, Ishmael Festus Jaja, Olufunke Eunice Ola-Davies, Temidayo Olutayo Omobowale, Adebowale Bernard Saba, Oluwafemi Omoniyi Oguntibeju, Evaristus Nwulia, Momoh Audu Yakubu

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引用次数: 0

Abstract

INTRODUCTION

Aluminum chloride (AlCl₃) exposure has been linked to neurotoxicity in various animal models, presenting significant concern to human health due to its potential implications in neurodegenerative diseases. Aluminum chloride is a widely recognized neurotoxin and has been used as an animal model of Alzheimer's disease via mechanisms linked with oxidative stress and inflammation. The study investigated the potential ameliorative effect of apigenin on AlCl₃-induced neurotoxicity in rats.

METHODS

Forty adult male Wistar rats were randomly divided into four different groups – control, AlCl₃ (100 mg/kg), apigenin (50 mg/kg) plus AlCl₃, and apigenin (50 mg/kg) alone administered orally for 14 days.

RESULTS

Our findings revealed AlCl₃ exposure induced significant neurobehavioral deficits, oxidative stress, neuroinflammation, and loss of the Purkinje cell layer of the cerebellum. Treatment with apigenin attenuated neuroinflammation and enhanced learning and memory with significant improvement in recognition index.

DISCUSSION

Apigenin demonstrates promising ameliorative effects against AlCl₃-induced neurotoxicity in rats.

Highlights

Aluminum chloride toxicity caused significant reduction in learning, exploration, and memory.
Aluminum chloride toxicity induced neurotoxicity, increased biomarkers of oxidative stress, neuroinflammation, and precipitated cognitive impairment.
Apigenin improved brain antioxidant, enhanced learning, exploration, and memory.

Abstract Image

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芹菜素减轻氧化应激、神经炎症和认知障碍，但增强氯化铝诱导的神经毒性大鼠的学习和记忆

在各种动物模型中，氯化铝（AlCl3）暴露与神经毒性有关，由于其对神经退行性疾病的潜在影响，对人类健康产生了重大影响。氯化铝是一种被广泛认可的神经毒素，并通过与氧化应激和炎症相关的机制被用作阿尔茨海默病的动物模型。本研究探讨芹菜素对alcl3诱导的大鼠神经毒性的潜在改善作用。方法40只成年雄性Wistar大鼠随机分为对照组、AlCl3 （100 mg/kg）组、芹菜素（50 mg/kg）加AlCl3组和芹菜素（50 mg/kg）单药组，连续口服14 d。结果：AlCl3暴露诱导了明显的神经行为缺陷、氧化应激、神经炎症和小脑浦肯野细胞层的丢失。芹菜素治疗可减轻神经炎症，增强学习和记忆，显著改善识别指数。芹菜素对alcl3诱导的大鼠神经毒性有良好的改善作用。氯化铝毒性导致学习、探索和记忆能力显著下降。氯化铝毒性诱导神经毒性，增加氧化应激、神经炎症和认知障碍的生物标志物。芹菜素改善大脑抗氧化，增强学习，探索和记忆。

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来源期刊

Alzheimer's & Dementia 医学-临床神经学

CiteScore

14.50

自引率

5.00%

发文量

299

审稿时长

3 months

期刊介绍： Alzheimer's & Dementia is a peer-reviewed journal that aims to bridge knowledge gaps in dementia research by covering the entire spectrum, from basic science to clinical trials to social and behavioral investigations. It provides a platform for rapid communication of new findings and ideas, optimal translation of research into practical applications, increasing knowledge across diverse disciplines for early detection, diagnosis, and intervention, and identifying promising new research directions. In July 2008, Alzheimer's & Dementia was accepted for indexing by MEDLINE, recognizing its scientific merit and contribution to Alzheimer's research.