DOI: 10.1007/s12640-017-9717-x Pages: 1-14
Article Type: ORIGINAL ARTICLE

N-Adamantyl-4-Methylthiazol-2-Amine Attenuates Glutamate-Induced Oxidative Stress and Inflammation in the Brain

1. Konyang University, Department of Biomedical Laboratory Science

2. University of Ulsan College of Medicine, Department of Biochemistry and Molecular Biology

3. Sema High School

4. Hallym University, Department of Biomedical Science and Research Institute for Bioscience and Biotechnology

Correspondence to:
Sung-Woo Cho
Tel: +82 2 3010 4278
Email: swcho@amc.seoul.kr

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Abstract

In this study, we explored the possible mechanisms underlying the neuroprotective and anti-oxidative effects of N-adamantyl-4-methylthiazol-2-amine (KHG26693) against in vivo glutamate-induced toxicity in the rat cerebral cortex. Our results showed that pretreatment with KHG26693 significantly attenuated glutamate-induced elevation of lipid peroxidation, tumor necrosis factor-α, interferon gamma, IFN-γ, interleukin-1β, nitric oxide, reactive oxygen species, NADPH oxidase, caspase-3, calpain activity, and Bax. Furthermore, KHG26693 pretreatment attenuated key antioxidant parameters such as levels of superoxide dismutase, catalase, glutathione, and glutathione reductase. KHG26693 also attenuated the protein levels of inducible nitric oxide synthase, neuronal nitric oxide synthase, nuclear factor erythroid 2-related factor 2, heme oxygenase-1, and glutamate cysteine ligase catalytic subunit caused by glutamate toxicity. Finally, KHG26693 mitigated glutamate-induced changes in mitochondrial ATP level and cytochrome oxidase c. Thus, KHG26693 functions as neuroprotective and anti-oxidative agent against glutamate-induced toxicity through its antioxidant and anti-inflammatory activities in rat brain at least in part.

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  • Accepted: Feb 28, 2017
  • Online: Mar 11, 2017
  • Revised: Feb 25, 2017

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