IMR Press / JIN / Volume 19 / Issue 2 / DOI: 10.31083/j.jin.2020.02.1236
Open Access Original Research
N-hydroxy-N'-(4-butyl-2-methylphenyl)-formamidine attenuates oxygen-glucose deprivation and reoxygenation-induced cerebral ischemia-reperfusion injury via regulation of microRNAs
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1 Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150081, P. R. China
2 First affiliated hospital, Heilongjiang University of Chinese Medicine, Harbin, 150040, P. R. China
3 Heilongjiang University of Chinese Medicine, Harbin, 150040, P. R. China
4 Xiamen Institute of Rare-Earth Materials, Xiamen, 361021, P. R. China
*Correspondence: ylzhu1111@126.com (Yulan Zhu); sunzhong_ren@163.com (Zhongren Sun)
These authors contributed equally.
J. Integr. Neurosci. 2020, 19(2), 303–311; https://doi.org/10.31083/j.jin.2020.02.1236
Submitted: 14 November 2019 | Revised: 16 April 2020 | Accepted: 30 April 2020 | Published: 30 June 2020
(This article belongs to the Special Issue Exploration of mechanisms in cortical plasticity)
Copyright: © 2020 Yang et al. Published by IMR press.
This is an open access article under the CC BY 4.0 license https://creativecommons.org/licenses/by/4.0/.
Abstract

Cerebral ischemia-reperfusion injury is a common complication that occurs during stroke treatment. Increasingly, microRNAs have been found to participate in the modulation of neuron function; however, the role of microRNAs in cerebral ischemia-reperfusion injury remains unclear. We developed a mechanism of cerebral ischemia-reperfusion injury using a cellular model of oxygen-glucose deprivation and reoxygenation-induced injury in human neuroblastoma SH-SY5Y cells. We found that treatment of oxygen-glucose deprivation and reoxygenation promoted the apoptosis of SH-SY5Y cells. Analysis of microRNAs sequencing revealed that the expression of microRNA-27a-5p was induced, and microRNA-29b-3p expression was inhibited in neuroblastoma cells exposed to oxygen-glucose deprivation and reoxygenation. Either inhibition of microRNA-27a-5p or overexpression of microRNA-29b-3p mitigated oxygen-glucose deprivation and reoxygenation-induced cellular apoptosis. Bach1 was authenticated as a target gene of microRNA-27a-5p. Also, microRNA-27a-5p mediated the expression of Bach 1 along with its downstream signaling. N-hydroxy-N'-(4-butyl-2-methylphenyl)-formamidine protected against oxygen-glucose deprivation and reoxygenation-induced apoptosis while decreasing miR-27a-5p expression and increasing microRNA-29b-3p expression. These results suggested that microRNA-27a-5p and microRNA-29b-3p may contribute to oxygen-glucose deprivation and reoxygenation-induced cellular injury. At the same time, N-hydroxy-N'-(4-butyl-2-methylphenyl)-formamidine protects SH-SY5Y cells against oxygen-glucose deprivation and reoxygenation-induced injury partly through the inhibition of microRNA-27-a-5p and promotion of the Bach1/HO-1 signaling pathway.

Keywords
Oxygen-glucose deprivation
miRNA-27a-5p
miRNA-29b-3p
N-hydroxy-N'-(4-butyl-2-methylphenyl)-formamidine
Bach 1
translational neuroscience
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