Kim, Jiae Cho, Chang Hun Hahn, Hoh-Gyu Choi, Soo-Young Cho, Sung-Woo 2024-01-20T02:32:27Z 2024-01-20T02:32:27Z 2021-09-05 2017-01 0361-9230 https://pubs.kist.re.kr/handle/201004/123250 We previously reported that N-adamantyl-4-methylthiazol-2-amine (KHG26693) suppresses amyloid beta (A beta)-induced neuronal oxidative damage in cortical neurons. Here we investigated the mechanism and antioxidative function of KHG26693 in the hippocampus of A beta-treated mice. KHG26693 significantly attenuated A beta-induced TNF-alpha and IL-1 beta enhancements. KHG26693 decreased A beta-mediated malondialdehyde formation, protein oxidation, and reactive oxygen species by decreasing the iNOS level. KHG26693 suppressed A beta-induced oxidative stress through a mechanism involving glutathione peroxidase, catalase, and GSH attenuation. A beta-induced MMP-2, cPLA2, and pcPLA2 expressions were almost completely attenuated by KHG26693 treatment, suggesting that A beta-induced oxidative stress reduction by KHG26693 is, at least partly, caused by the downregulation of MMP-2 and cPLA2 activation. Compared with A beta treatment, KHG26693 treatment upregulated Nrf2 and HO-1 expressions, suggesting that KHG26693 protects the brain from AP-induced oxidative damage, likely by maintaining redox balance through Nrf2/HO-1 pathway regulation. KHG26693 significantly attenuated A beta-induced oxidative stress in the hippocampus of A beta-treated mice. (C) 2016 Elsevier Inc. All rights reserved. English PERGAMON-ELSEVIER SCIENCE LTD CYTOSOLIC PHOSPHOLIPASE A(2) ALZHEIMERS-DISEASE RAT MODEL DERIVATIVES EXPRESSION DAMAGE BRAIN TRANSCRIPTION ACTIVATION OLIGOMERS Neuroprotective effects of N-adamantyl-4-methylthiazol-2-amine against amyloid beta-induced oxidative stress in mouse hippocampus Article 10.1016/j.brainresbull.2016.10.010 1 BRAIN RESEARCH BULLETIN, v.128, pp.22 - 28 BRAIN RESEARCH BULLETIN 128 22 28 scie scopus 000392354000004 2-s2.0-84995814830 Neurosciences Neurosciences & Neurology Article CYTOSOLIC PHOSPHOLIPASE A(2) ALZHEIMERS-DISEASE RAT MODEL DERIVATIVES EXPRESSION DAMAGE BRAIN TRANSCRIPTION ACTIVATION OLIGOMERS Amyloid beta Alzheimer&apos s disease Oxidative stress N-Adamantyl-4-methylthiazol-2-amine