Avicularin Attenuates Memory Impairment in Rats with Amyloid Beta-Induced Alzheimer’s Disease

Amyloid-beta-induced Alzheimer’s disease (AD) and its further complications are well-established models in preclinical studies and demonstrated by many researchers. Intracerebroventricular injection of Aβ produces brain malfunction, including neurodegeneration and memory impairment. Avicularin is a bioactive flavonoid that has been found to prevent oxidative stress and proinflammatory cytokines. Alzheimer’s disease treatment may benefit from inhibiting amyloid-beta and its related complications. Hence, by considering multiple actions of avicularin, including antioxidant and anti-inflammatory, we demonstrated the neuroprotective action of avicularin against amyloid beta-induced neurotoxicity. Aβ1–42 (1 µg/µl) was dissolved in phosphate buffer solution (pH7.4) and incubated at 37 °C for 3 days to induce aggregation. A single intracerebroventricular (i.c.v.) injection of the Aβ1-42 was given to the animals utilizing stereotaxic equipment. Avicularin was dissolved in 0.5% sodium carboxymethyl cellulose (CMC), and treatment was given to the animals for 21 days at a dose of (25, 50, and 100 mg/kg, p.o.) after Aβ1-42 peptide (i.c.v.) injection. Several behavioral studies, acetylcholinesterase activity, oxidative stress, TNFα, IL-6, IL-1β, and expression of BDNF and amyloid-beta were measured. Avicularin treatment (50 and 100 mg/kg) showed cognition enhancement activity in behavioral studies and could reverse the effects of amyloid beta-induced inflammatory response and excessive oxidative stress. Furthermore, the findings reveal that avicularin can halt AD progression by targeting BDNF and amyloid-beta levels in the brain, suggesting that avicularin could be used for Alzheimer’s disease treatment.