Okoh, Victor Ifeanyi, Campos, Hericles Mesquita, Yasmin de Oliveira Ferreira, Pâmela, Pereira, Robbert Mota, Souza Silva, Yohanny, Arruda, Evilanna Lima, Pagliarani, Barbara, de Almeida Ribeiro Oliveira, Gerlon, Lião, Luciano Morais, Franco dos Santos, Gabriel, Vaz, Boniek Gontijo, Sabino, José Ricardo, Alcantara dos Santos, Fernanda Cristina, Costa, Elson Alves, Tarozzi, Andrea, Menegatti, Ricardo, and Ghedini, Paulo César
Objectives: To evaluate whether the glycosylation of chrysin (CHR) enhances its protective effects against aluminum-induced neurotoxicity. Methods: To compare the antioxidant, anticholinesterase, and behavioral effects of CHR with its glycosylated form (CHR bonded to β-d-glucose tetraacetate, denoted as LQFM280), we employed an integrated approach using both in vitro (SH-SY5Y cells) and in vivo (aluminum-induced neurotoxicity in Swiss mice) models. Key findings: LQFM280 demonstrated higher antioxidant activity than CHR in both models. Specifically, LQFM280 exhibited the ability to exert antioxidant effects in the cytoplasm of SH-SY5Y cells, indicating its competence in traversing neuronal membranes. Remarkably, LQFM280 proved more effective than CHR in recovering memory loss and counteracting neuronal death in the aluminum chloride mice model, suggesting its increased bioavailability at the brain level. Conclusions: The glycosylation of CHR with β-d-glucose tetraacetate amplifies its neuroprotective effects, positioning LQFM280 as a promising lead compound for safeguarding against neurodegenerative processes involving oxidative stress. Graphical Abstract [ABSTRACT FROM AUTHOR]