Palabiyik-Yuceli̇k S.S.Zeybek N.D.Cinar I.Akpinar E.Bahador Zırh E.Si̇pahi̇ H.Halici Z.2023-04-112023-04-122023-04-112023-04-122023-03-0113826689https://hdl.handle.net/20.500.12597/4029Chronic aluminium(Al) exposure can affect the antioxidant and glutaminergic systems through N-methyl-D-aspartate receptors (NMDAR). This study was aimed to investigate the neurotoxic effect of Al through different mechanisms in rat hippocampus and to evaluate the protective role of epigallocatechin gallate (EGCG), a well-known antioxidant, with simultaneous administration of Al,as well as post-treatment after Al exposure.For this purpose, aluminum chloride(AlCl3) was administered simultaneously with two different EGCG doses for 8 weeks as the first part of the study.In the second part of the study, after 4 weeks of AlCl3 pre-administration, two different EGCG doses were also administered during four additional weeks as post-treatment.Al administration led to oxidative stress and increased acetylcholinesterase levels.NMDAR subunit mRNA expressions were down-regulated by Al, which was apparent in NMDAR1/2B subunits.Simultaneous EGCG treatment has shown a better neuroprotective effect in terms of these mechanisms and represents novel approach for the prevention of neurodegenerative diseases likely to be induced by Al.falseAluminum | Epigallocatechin gallate | Neurotoxicity | NMDARArticle10.1016/j.etap.2023.1040612-s2.0-8514581889436621558