BMB Reports Papers in Press available online.

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

Protective effect of 3-(naphthalen-2-yl(propoxy)methyl)azetidine hydrochloride on hypoxia-induced toxicity by suppressing microglial activation in BV-2 cells
Jiae Kim1,#, Su-Min Kim2,#, Jung-Min Na1, Hoh-Gyu Hahn3, Sung-Woo Cho1,#, Seung-Ju Yang2,*,#
1Department of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 05505, Korea,
2Department of Biomedical Laboratory Science, Konyang University, Daejeon 35365, Korea,
3Chemical Kinomics Research Center, Korea Institute of Science and Technology, Seoul 02456, Korea
We recently reported the anti-inflammatory effects of 3-(naphthalen-2-yl(propoxy)methyl)azetidine hydrochloride (KHG26792) on the ATP-induced activation of the NFAT and MAPK pathways through the P2X7 receptor in microglia. To further investigate the underlying mechanism of KHG26792, we studied its protective effects on hypoxia-induced toxicity in microglia. The administration of KHG26792 significantly reduced the hypoxia-induced expression and activity of caspase-3 in BV-2 microglial cells. KHG26792 also reduced hypoxia-induced inducible nitric oxide synthase protein expression, which correlated with reduced nitric oxide accumulation. In addition, KHG26792 attenuated hypoxia-induced protein nitration, reactive oxygen species production, and NADPH oxidase activity. These effects were accompanied by the suppression of hypoxia-induced protein expression of hypoxia-inducible factor 1-alpha and NADPH oxidase-2. Although the clinical relevance of our findings remains to be determined, these data results suggest that KHG26792 prevents hypoxia-induced toxicity by suppressing microglial activation.
Abstract, Accepted Manuscript(in press) [Submitted on October 6, 2016, Accepted on October 19, 2016]
  Copyright © KSBMB. All rights reserved. / Powered by, Ltd