Cakir, MuratDuzova, HalilTekin, SuatTaslidere, ElifKaya, Gul BusraCigremis, YilmazOzgocer, Tuba2024-08-042024-08-0420170024-32051879-0631https://doi.org/10.1016/j.lfs.2017.03.022https://hdl.handle.net/11616/97762Aim: In recent studies, it has been shown that the Transient Receptor Potential Melastatin-2 Channels (TRPM2) and Phospholipases A2 (PLA(2)) inhibitors may have a protective effect on neurons. This study was aimed to investigate the protective effect of TRPM2 and PLA(2) inhibitor N-(p-amylcinnamoyl) Anthranilic Acid (ACA) in a neurodegenerative model induced by Okadaic Acid (OKA). Main methods: OKA (200 ng/10 mu l) was administered bilateral intracerebroventricularly as a single injection. Key findings: OKA-treated rats showed significant impairments of spatial memory in Morris Water Maze Test. OKA-induced memory-impaired rats showed increased numbers of degenerated neurons and Caspase-3, tau phosphorylated ser396, beta-amyloid positive cells in the hippocampus and cerebral cortex. Furthermore, OKA-treated rats exhibited significantly increased MDA, TNF-alpha levels, and decreased SOD, GSH-PX enzyme activates and GSH levels of the tissues. ACA administration ameliorated OKA-induced memory impairment in rats. The ACA treatment also increased SOD and GSH-PX enzyme activation and GSH levels, and conversely decreased the levels of MDA, TNF-alpha. It was found that the numbers of the degenerated neurons and Caspase-3 positive cells of cortex and hippocampus regions were significantly reduced. Significance: ACA administration attenuates the oxidative stress and neuroinflammation of OKA-induced neurodegeneration; and ameliorates the cognitive decline and neurodegeneration. (C) 2017 Elsevier Inc. All rights reserved.eninfo:eu-repo/semantics/closedAccessOkadaic acidN-(p-amylcinnamoyl) anthranilic acid (ACA)NeurodegenerationTRPM2 channelPhospholipases A(2)Alzheimer's diseaseArticle17610202836384110.1016/j.lfs.2017.03.0222-s2.0-85016397485Q1WOS:000400537500002Q2