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The isoflavones and extracts from Maclura tricuspidata fruit protect against neuronal cell death in ischemic injury via induction of Nox4-targeting miRNA-25, miRNA-92a, and miRNA-146a

Authors
Hong, SungeunKwon, JaeyoungNguyen Tuan HiepSim, Su JinKim, NahyunKim, Kyeong HoLee, DonghoMar, Woongchon
Issue Date
1월-2018
Publisher
ELSEVIER
Keywords
Maclura tricuspidata; MiroRNAs; Oxygen-glucose deprivation/reoxygenation plus glucose; Middle cerebral artery occlusion/reperfusion; NADPH oxidase; MAPkinase
Citation
JOURNAL OF FUNCTIONAL FOODS, v.40, pp.785 - 797
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF FUNCTIONAL FOODS
Volume
40
Start Page
785
End Page
797
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/78396
DOI
10.1016/j.jff.2017.12.011
ISSN
1756-4646
Abstract
This study evaluated the neuroprotective effects 50% EtOH extract of Maclura tricuspidata fruits (FME50) and isolated compounds, cudraisoflavone I (CFI), and cudraisoflavone H (CFH), on ischemic damage in in vitro model and in vivo model of cerebral ischemia. FME50, CFI, and CFH inhibited OGD/R + glucose-induced neuronal cell death, ROS generation, and Nox4 expression via induction of Nox4-targeting miRNA-25, miRNA-92a, and miRNA-146a in SH-SY5Y cells. Also, FME50 suppressed OGD/R + glucose-induced activation of ASK1-JNK1/p38 MAPK signal cascade. Furthermore, FME50 significantly reduced the MCAO/R-induced brain infarct, Nox4 expression via induction of Nox4-targeting three miRNAs. Additionally, FME50 suppressed MCAO/R-induced MAPK signal pathway. These results demonstrate that FME50, CFI, and CFH exert neuroprotective effects via Nox4 inhibition by the induction of Nox4-targeting miRNAs and inhibition of MAPK signal cascade, suggesting that they might be possible candidates for the treatment of cerebral ischemia.
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