Gallic acid and hesperidin elevate neurotransmitters level and protect against oxidative stress, inflammation and apoptosis in aluminum chloride-induced Alzheimer's disease in rats

Abstract

Background/AimGallic acid and metformin are plant-derived compounds with biological effects. The present study aimed to evaluate the protective effect of gallic acid and hesperidin against aluminium chloride (AlCl3)-induced Alzheimer's disease in Wistar rats. MethodsThirty-five male rats were randomly distributed into seven groups of five animals each. Group 1 was administered distilled water only, throughout the study. Animals in groups 2-5 received AlCl3 (100 mg/kg/day) throughout the study. Groups 3, 4 and 5 were administered 100 mg/kg/day gallic acid,100 mg/kg/day hesperidin and 10 mg/kg/day donepezil respectively, in addition to 100 mg/kg/day AlCl3. Groups 6 and 7 were treated with 100 mg/kg/day gallic acid only and 100 mg/kg/day hesperidin only, respectively. Treatments were oral, with distilled water as vehicle. The study lasted for 21 days. Cognitive impairment was assessed by Morris water maze and Y maze on the 21st day. Activities of cholinesterases and antioxidant enzymes, as well as levels of reduced glutathione, malondialdehyde, neurotransmitters, caspase-3 and cytokines were evaluated in the brain. ResultsResults showed that AlCl3 caused an increase in the retention latency time and reduction in the percentage alternation index in experimental animals. However, treatment with gallic acid or hesperidin prevented cognitive impairment occasioned by AlCl3. Moreover, gallic acid or hesperidin significantly prevented deficits in neurotransmission, oxidative stress and inflammation, while also lowering brain caspase-3 level. These observations were corroborated by results of histopathological evaluation. ConclusionResults from this study suggest that both gallic acid and hesperidin conferred significant protection against AlCl3–induced Alzheimer's disease in rats, and their consumption could be relevant in delaying the onset of the disease.