Pharmacological effects of Ibuprofen on learning and memory, Muscarinic receptors genes expression and APP isoforms levels in Prefrontal cortex of AlCl3induced toxicity mouse model

Abstract

Aluminium metal (Al) has been implicated in etiology of many neurodegenerative diseases, most commonly the Alzheimer’s disease (AD). Al causes the biochemical defects, by affecting the neurotransmitters levels, causes conformational changes in amyloid protein and increases amyloid accumulation in brain. There exists an epidemiological linked between chronic exposure to Al and the incidence of AD. Aim: This study was aimed at evaluating neuroprotective effect of Ibuprofen (IBU) (25mg/kg/day for 12 days) in AlCl3induced (150mg/kg/day for 12 days) toxicity. Methods: Treated mice were subjected to learning and memory tests. Cholinergic muscarinic receptors (mAChR; M1M5) and APP isofroms (APP695, APP770 and APP common) gene expression were carried out from the prefrontal cortex area. Results: Profound effect on learning and memory was observed in IBU treated group along with enhanced expression of M1 mAChR (0.40±0.03; p<0.01) compared to AlCl3inducedtoxicity group (0.05±0.02). Fear memory was improved in IBU treated group (89.68±2.58, p<0.01) as compared to AlCl3induced toxicity group (54.58±8.21). Discrimination index in social novelty test in IBU treated group was improved (81.13±8.71; p<0.05), compared to AlCl3induced toxicity group (46.28±5.55).Similarly recognition memory of IBU treated group in novel object recognition test was retained (66.85±5.60; p<0.05) compared to AlCl3induced toxicity group (33.06±11.80). Conclusion: Ibuprofen demonstrated memory enhancing effect, however, its effect on the APP isoforms expressions in prefrontal cortex needs further studies.