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MicroRNA-579-3p Exerts Neuroprotective Effects Against Ischemic Stroke via Anti-Inflammation and Anti-Apoptosis

Authors Jia J, Cui Y, Tan Z, Ma W, Jiang Y

Received 1 December 2019

Accepted for publication 30 March 2020

Published 12 May 2020 Volume 2020:16 Pages 1229—1238

DOI https://doi.org/10.2147/NDT.S240698

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Prof. Dr. Yuping Ning


Jiaoying Jia, Yan Cui, Zhigang Tan, Wenjia Ma, Yugang Jiang

Department of Neurosurgery, The Second Xiangya Hospital of Central South University, Changsha City, Hunan Province 410011, People’s Republic of China

Correspondence: Yugang Jiang
Department of Neurosurgery, The Second Xiangya Hospital of Central South University, Changsha City, Hunan Province 410011, People’s Republic of China
Tel +8673185295880
Email jiangyugang123@csu.edu.cn

Background/Aims: Multiple studies have found that microRNAs (miRNAs) are involved in the development of cerebral ischemia. MiR-579-3p can inhibit inflammatory responses and apoptosis, leading to ischemia/reperfusion (I/R) damage. However, the mechanism of how miR-579-3p actions in brain I/R injury remains unclear. This study aimed to investigate the mechanism of the role of miR-579-3p in brain I/R injury.
Methods: A rat model of cerebral ischemia–reperfusion injury was established by suture method. The effects of miR-579-3p on cerebral infarction size, brain water content, and neurological symptoms were evaluated. Flow cytometry was used to detect apoptosis. ELISA was used to detect the level of inflammatory factors. Western blot was used to detect the expression of P65, NCOA1, Bcl-2 and Bax. The relationship between miR-579-3p and NCOA1 was analyzed by bioinformatics analysis and luciferase assay.
Results: Overexpression of miR-579-3p reduced infarct volume, brain water content and neurological deficits. Overexpression of miR-579-3p inhibited the expression level of the inflammatory cytokines, such as TNF-α, IL-6, COX-2 and iNOS, and increased the expression level of IL-10. MiR-579-3p overexpression inhibited NF-кB activity by reducing NRIP1. In addition, miR-579-3p could reduce the apoptotic rate of cortical neurons. Overexpression of miR-579-3p inhibited the activity of caspase-3, increased the expression level of anti-apoptotic gene Bcl-2 in neurons, and decreased the expression level of apoptotic gene Bax.
Conclusion: miR-579-3p can be used to treat brain I/R injury, and its neuroprotective effect may be ascribed to the reduction of inflammation and apoptosis.

Keywords: ischemia/reperfusion, miR-579-3p, inflammation, apoptosis

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