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N-Adamantyl-4-methylthiazol-2-amine suppresses glutamate-induced autophagic cell death via PI3K/Akt/mTOR signaling pathways in cortical neurons
Seung-Ju Yang1,# (Professor), A Reum Han2,# (Graduate student), Hye-Rim Choi1 (Graduate student), Kyouk Hwang2 (College student), Eun-A Kim2 (Research worker), Soo Young Choi3 (Professor), Sung-Woo Cho 2,* (Professor)
1Biomedical Laboratory Science, Konyang University,
2Biochemistry and Molecular Biology, University of Ulsan College of Medicine,
3Biomedical Science and Research Institute for Bioscience and Biotechnology, Hallym University
Abstract
We recently reported that N-adamantyl-4-methylthiazol-2-amine (KHG26693) attenuates glutamate-induced oxidative stress and inflammation in the brain. In this study, we investigated KHG26693 as a therapeutic agent against glutamate-induced autophagic death of cortical neurons. Treatment with KHG26693 alone did not affect the viability of cultured cortical neurons but was protective against glutamate-induced cytotoxicity in a concentration-dependent manner. KHG26693 attenuated the glutamate-induced increase in protein levels of LC3, beclin-1, and p62. Whereas glutamate decreased the phosphorylation of PI3K, Akt, and mTOR, these levels were restored by treatment with KHG26693. These results suggest that KHG26693 inhibits glutamate-induced autophagy by regulating PI3K/Akt/mTOR signaling. Finally, KHG26693 treatment also attenuated glutamate-induced increases in reactive oxygen species, glutathione, glutathione peroxidase, and superoxide dismutase levels in cortical neurons, indicating that KHG26693 also protects cortical neurons against glutamate-induced autophagy by regulating the reactive oxygen species scavenging system.
Abstract, Accepted Manuscript(in press) [Submitted on March 20, 2020, Accepted on April 20, 2020]
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