article · BMC Pharmacology and Toxicology
Chronic exposure to aluminium poses a risk to cognitive function by causing oxidative damage and inflammation in the brain. This study assessed whether hesperidin, a compound found in citrus fruits, can counter aluminium chloride toxicity in male mice. Mice were administered aluminium chloride alone or alongside daily doses of hesperidin at 50 or 100 milligrams per kilogram over 28 days. Exposure to aluminium chloride led to poor spatial working memory, decreased exploratory activity, and signs of neurochemical stress, including depleted antioxidant enzymes and increased inflammatory markers. Co-administration of hesperidin reversed these behavioural and biochemical deficits in a dose-dependent manner. In particular, the higher dose restored memory performance, raised antioxidant enzyme levels, reduced lipid peroxidation, and curbed key inflammatory cytokines. These findings demonstrate that hesperidin protects against aluminium-induced neurotoxicity in an animal model by boosting endogenous antioxidants and limiting brain inflammation.
Environmental exposure to heavy metals such as aluminium contributes to neurodegeneration and cognitive impairment. Identifying naturally derived compounds that mitigate these toxic effects provides insights into protective strategies. By demonstrating that hesperidin dampens brain inflammation and oxidative stress while preserving memory in mice, this research highlights potential mechanisms for countering metal-induced neural damage.
This research represents early-stage preclinical work in a rodent model. The findings could eventually interest nutraceutical or pharmaceutical developers exploring neuroprotective agents against environmental toxin exposure or cognitive decline. However, real-world application remains distant, as the results support only further preclinical evaluation rather than direct therapeutic use.
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Chronic aluminium exposure is an established environmental risk factor for cognitive decline, acting largely through oxidative injury and glial-driven inflammation in the brain. Hesperidin, a citrus flavanone glycoside with reported antioxidant and anti-inflammatory activity, was examined for protection against aluminium chloride (AlCl₃) neurotoxicity. Male Swiss albino mice ( n = 5 per group) received AlCl₃ alone or AlCl₃ together with hesperidin at 50 or 100 mg/kg by oral gavage for 28 days, alongside a vehicle-treated control. Spatial working memory and exploratory behaviour were assessed using the Y-maze and open field tests, and brain tissue was analysed for superoxide dismutase (SOD), catalase, glutathione S-transferase (GST), malondialdehyde (MDA), interleukin-1β (IL-1β), and tumour necrosis factor-alpha (TNF-α). AlCl₃ produced consistent behavioural impairment, with reduced rearing and line crossing, prolonged centre-square duration, and a fall in correct Y-maze alternation by day 28 compared to control ( p < 0.05). Total arm entries were not significantly reduced by AlCl₃, indicating that the alternation deficit did not reflect altered exploratory activity. These deficits were accompanied by depleted SOD, catalase, and GST activity, elevated MDA, and pronounced increases in IL-1β and TNF-α. Hesperidin reversed this profile in a dose-related manner. The 100 mg/kg dose significantly restored line crossing and Y-maze alternation, shortened centre-square duration, raised antioxidant enzyme activity, lowered lipid peroxidation, and suppressed both cytokines compared to the AlCl₃-only group ( p < 0.05), while the lower dose produced intermediate effects. These findings indicate that hesperidin protects the mouse brain against aluminium-induced cognitive and biochemical damage, with behavioural recovery accompanied by reinforcement of endogenous antioxidant enzyme activity and reduction of pro-inflammatory cytokine levels. The upstream signalling responsible was not measured in this study, and the findings support further preclinical evaluation rather than any claim of therapeutic potential.
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DOI: 10.1186/s40360-026-01209-w
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