Protective effects of chrysin against the neurotoxicity induced by aluminium: In vitro and in vivo studies. (15th January 2022)

• Record Type: Journal Article
• Authors: Campos, Hericles Mesquita; da Costa, Michael; da Silva Moreira, Lorrane Kelle; da Silva Neri, Hiasmin Franciely; Branco da Silva, Cinthia Rio; Pruccoli, Letizia; dos Santos, Fernanda Cristina Alcantara; Costa, Elson Alves; Tarozzi, Andrea; Ghedini, Paulo César
• Is Part Of: Toxicology. Volume 465(2022)
• Publication Date: 2022-01-15
• Subjects: Aluminium -- Neurotoxicity -- Oxidative stress -- Antioxidant -- Chrysin; Toxicology -- Periodicals; Chemicals -- Physiological effect -- Periodicals; 615.9005
• DOI: 10.1016/j.tox.2021.153033
• Languages: English
• ISSNs: 0300-483X

Abstract

Abstract: Chronic exposure to aluminium (Al) can contribute to the progression of several neurological and neurodegenerative diseases. Al is a metal that promotes oxidative damage leading to neuronal death in different brain regions with behavior, cognition, and memory deficits. Chrysin is a flavonoid found mainly in honey, passion fruit, and propolis with antioxidant, anti-inflammatory, and cytoprotective properties. In this study, we used an integrated approach of in vitro and in vivo studies to evaluate the antioxidant and neuroprotective effects of chrysin against the neurotoxicity elicited by aluminium chloride (AlCl3 ). In in vitro studies, chrysin (5 μM) showed the ability to counteract the early oxidative stress elicited by tert-butyl hydroperoxide, an oxidant that mimics the lipid peroxidation and Fenton reaction in presence of AlCl3 as well as the late necrotic death triggered by AlCl3 in neuronal SH-SY5Y cells. In vivo studies in a mouse model of neurotoxicity induced by chronic exposure to AlCl3 (100 mg/kg/day) for ninety days then corroborated the antioxidant and neuroprotective effect of chrysin (10, 30, and 100 mg/kg/day) using the oral route. In particular, chrysin reduced the cognitive impairment induced by AlCl3 as well as normalized the acetylcholinesterase and butyrylcholinesterase activities in the hippocampus. In parallel, chrysin counteracted the oxidative damage, in terms of lipid peroxidation, protein carbonylation, catalase, and superoxide dismutase impairment, in the brain cortex and hippocampus. Lastly, necrotic cells frequency in the same brain regions was also decreased by chrysin. These results highlight the ability of chrysin to prevent the neurotoxic effects associated with chronic exposure to Al and suggest its potential use as a food supplement for brain health.