Neurobehavioural Changes and Oxidative Damage due to Aluminium Chloride-Induced Neurotoxicity in Adult Female Wistar Rats: <i>Phoenix Dactylifera</i> L. Fruit to the Rescue

Background: Aluminium-induced neurotoxicity has become a subject of substantial concern because of its consequential effects, including its potential role in neurodegenerative disease pathogenesis. It is thought to occur through multiple mechanisms including the generation of reactive oxygen species and the disruption of cellular homeostasis leading to neuronal damage and dysfunction. However, despite growing evidence of aluminium-induced neurotoxicity, the precise mechanisms underlying its effects and potential therapeutic strategies remain incompletely understood. Its manifestations therefore need to be explored so that its adverse effects can be attenuated. Methods: In the present study, we investigated the neurotoxic effects of aluminium chloride (AlCl 3 ) in relation to neurobehavioural changes and oxidative damage. We also assessed the therapeutic role and protective effects of aqueous extract of Phoenix dactylifera L. fruit (AEPDLF) on antioxidant levels (catalase and superoxide dismutase) and neurobehavioural patterns in adult female Wistar rats. Results: Thirty adult female Wistar rats were divided into five groups (N =30, each group n =6). Control group (A) rats received 2 mL/kg body weight/day (bw/d) of distilled water, and rats in the other four groups (B, C, D, and E) received 200 mg/kg bw/d of AlCl 3 for 28 days. In addition, the treated groups (C, D, and E) received 250, 500, and 1000 mg/kg bw/d, respectively, of AEPDLF for 28 days. On the last day of administration, neurobehavioural assessments were performed. Rats were then sacrificed and brains were harvested and homogenised for biochemical assays. With AlCl 3 treatment, body weight decreased more than brain weight. There was also significantly reduced locomotion with AlCl 3 treatment; however, dose-dependent amelioration was observed with AEPDLF. Although group B had significantly fewer entries into baited arms, and more entries into non-baited arms than group A in the radial arm maze, these changes were ameliorated in groups C, D, and E in an AEPDLF dose-dependent manner. Furthermore, AlCl 3 treatment lowered catalase and superoxide dismutase levels, and these changes were mitigated by AEPDLF in a dose-dependent fashion. Conclusion: The protective capacity of AEPDLF in female rats most efficiently combatted neurotoxicity at 1000 mg/kg bw/d in response to chronic (28 d) AlCl 3 exposure.