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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

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
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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