Antioxidant, anti-inflammatory, and neuroprotective role of pterostilbene in attenuating Alzheimer-like pathology in AlCl3-induced rats’ model of Alzheimer's disease

Background: Alzheimer’s disease (AD) is a degenerative neurological ailment marked by the accumulation of aberrant protein deposits in the brain, including beta-amyloid (Aβ) plaques and neurofibrillary tangles (NFTs) formed from tau protein. Objectives: to evaluate the potential preventive effects of pterostilbene against aluminum chloride-induced Alzheimer's disease in rats, examining its influence on oxidative and inflammatory markers and histopathological changes alterations. Method: involved the random creation of five groups, each consisting of eight rats. Induction of Alzheimer's disease was achieved using AlCl3 (70 mg/kg, intraperitoneally) for 30 days, followed by treatment with PTE (50 and 100 mg/kg, orally) or donepezil (0.1 mg/kg, orally) for 14 days, except for the control group, which received normal saline for the initial 30 days, followed by the vehicle alone. The open field test was employed for the neurobehavioral assessment of the rats. A biochemical examination was subsequently conducted utilizing ELISA kits to demonstrate the impact of PTE on the levels of 8-Epi-Prostaglandin F2α (8-epi-PGF2α), IL-1β, and TNF-α, and a colorimetric kit to demonstrate the impact of PTE on the total antioxidant capacity (TAOC). Additional validations were conducted through histopathological evaluation of the cortex by Congo red stain. Result: Exposure to AlCl3 significantly elevated 8-epi-PGF2α, IL-1β and TNF-α while markedly decreasing TAOC. These results were reversed in PTE-treated rats. Histopathological assessment of the cortex in rat brains produced by AlCl3 demonstrated pathological changes. such pathology was not present in rats administered PTE. Conclusion: A conducted study showed the anti-AD activity of PTE by reducing oxidative stress and inflammation, and amyloidosis, possibly by decreasing 8-epi-PGF2α, IL-1β and TNF-α and increasing TAOC.