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

Alzheimers Dement. 2025 May;21(5):e70223. doi: 10.1002/alz.70223.

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.

PMID:40318207 | DOI:10.1002/alz.70223