Research Paper|Volume 12, Issue 13|pp 12869—12895

miR-183-5p alleviates early injury after intracerebral hemorrhage by inhibiting heme oxygenase-1 expression

Yu Wang¹, Yuejia Song², Yuxin Pang¹, Zihan Yu¹, Wei Hua¹, Yunhe Gu¹, Jiping Qi¹, He Wu¹

¹Department of Pathology, First Clinical Hospital, Harbin Medical University, Harbin 150001, China
²Department of Endocrinology, First Clinical Hospital, Harbin Medical University, Harbin 150001, China

* Equal contribution

Received: January 11, 2020Accepted: May 18, 2020Published: June 29, 2020

Copyright © 2020 Wang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Differences in microRNA (miRNA) expression after intracerebral hemorrhage (ICH) have been reported in human and animal models, and miRNAs are being investigated as a new treatment for inflammation and oxidative stress after ICH. In this study, we found that microRNA-183-5p expression was decreased in the mouse brain after ICH. To investigate the effect of miRNA-183-5p on injury and repair of brain tissue after ICH, saline, miRNA-183-5p agomir, or miRNA-183-5p antagomir were injected into the lateral ventricles of 8-week-old mice with collagenase-induced ICH. Three days after ICH, mice treated with exogenous miRNA-183-5p showed less brain edema, neurobehavioral defects, inflammation, oxidative stress, and ferrous deposition than control mice. In addition, by alternately treating mice with a heme oxygenase-1 (HO-1) inducer, a HO-1 inhibitor, a nuclear factor erythroid 2-related factor (Nrf2) activator, and Nrf2 knockout, we demonstrated an indirect, HO-1-dependent regulatory relationship between miRNA-183-5p and Nrf2. Our results indicate that miRNA-183-5p and HO-1 are promising therapeutic targets for controlling inflammation and oxidative damage after hemorrhagic stroke.