α-bisabolol β-D-fucopyranoside inhibits β-amyloid (Aβ)25–35 induced oxidative stress in Neuro-2a cells via antioxidant approaches

Abstract

β-amyloid (Aβ)25–35 peptide-induced oxidative stress is one of the primary reasons for the development of Alzheimer’s disease (AD). In the present study, α-bisabolol β-D-fucopyranoside (ABFP) was evaluated for its protective effect against β-amyloid (Aβ)25–35 peptide-induced toxicity in Neuro-2a cells. The results of the current study revealed that ABFP inhibits acetylcholinesterase, apart from reducing the formation of lipid peroxides, protein carbonyls, and nitric oxides in Neuro-2a cells during the treatment of β-amyloid (Aβ)25–35 peptide. Additionally, ABFP effectively prevented the mitochondrial membrane damage induced by the β-amyloid (Aβ)25–35 peptide in Neuro-2a cells. Furthermore, ABFP was found to significantly inhibit caspase 3 production in Neuro-2a cells, which was confirmed through AO/EtBr, Annexin-V/FITC, and PI fluorescent microscopic images, indicating that ABFP has anti-apoptotic properties. In addition, ABFP also increased the anti-apoptotic protein expression and protected the Neuro-2a cell from β-amyloid (Aβ)25–35 peptide-induced toxicity. The in silico molecular docking analysis of ABFP with GSK-3beta showed that it was able to bind with Asn 186, Asp 200, and Lys 183 residues of the enzyme. Overall, the results suggest that ABFP acts as a potent drug against oxidative stress-mediated cell death in AD.