Mulberrofuran G Protects Ischemic Injury-induced Cell Death via Inhibition of NOX4-mediated ROS Generation and ER Stress
- Authors
- Hong, Sungeun; Kwon, Jaeyoung; Kim, Dong-Woo; Lee, Hak Ju; Lee, Dongho; Mar, Woongchon
- Issue Date
- 2월-2017
- Publisher
- WILEY
- Keywords
- mulberrofuranG; neuroprotection; oxygen-glucose deprivation/reoxygenation; middle cerebral artery occlusion/reperfusion; NADPH oxidase; endoplasmic reticulum stress
- Citation
- PHYTOTHERAPY RESEARCH, v.31, no.2, pp.321 - 329
- Indexed
- SCIE
SCOPUS
- Journal Title
- PHYTOTHERAPY RESEARCH
- Volume
- 31
- Number
- 2
- Start Page
- 321
- End Page
- 329
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/84826
- DOI
- 10.1002/ptr.5754
- ISSN
- 0951-418X
- Abstract
- The aim of this study was to investigate the neuroprotective effect of mulberrofuran G (MG) in in vitro and in vivo models of cerebral ischemia. MG was isolated from the root bark of Morus bombycis. MG inhibited nicotinamide adenine dinucleotide phosphate oxidase (NOX) enzyme activity and oxygen-glucose deprivation/reoxygenation (OGD/R)-induced NOX4 protein expression in SH-SY5Y cells. MG inhibited the expression of activated caspase-3 and caspase-9 and cleaved poly adenine dinucleotide phosphate-ribose polymerase in OGD/R-induced SH-SY5Y cells. In addition, MG protected OGD/R-induced neuronal cell death and inhibited OGD/R-induced reactive oxygen species generation in SH-SY5Y cells. In in vivo model, MG-treated groups (0.2, 1, and 5 mg/kg) reduced the infarct volume in middle cerebral artery occlusion/reperfusion-induced ischemic rats. The MG-treated groups also reduced NOX4 protein expression in middle cerebral artery occlusion/reperfusion-induced ischemic rats. Furthermore, protein expression of 78-kDa glucose-regulated protein/binding immunoglobulin protein, phosphorylated IRE1a, X-box-binding protein 1, and cytosine enhancer binding protein homologous protein, mediators of endoplasmic reticulum stress, were inhibited in MG-treated groups. Taken together, MG showed protective effect in in vitro and in vivo models of cerebral ischemia through inhibition of NOX4-mediated reactive oxygen species generation and endoplasmic reticulum stress. This finding will give an insight that inhibition of NOX enzyme activity and NOX4 protein expression could be a new potential therapeutic strategy for cerebral ischemia. Copyright (C) 2016 John Wiley & Sons, Ltd.
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