Studies paid much attention to the role of microRNAs (miRNAs) in hypoxic-ischemic brain damage (HIBD) but not much to miR-139-5p. Thus, this study is to uncover the potential role of miR-139-5p in HIBD and its mechanisms.
Rat HIBD models were established by Rice-Vannucci method. Rats were injected with miR-139-5p agomir and si-histone deacetylase 4 (HDAC4) to explore their roles in HIBD. For further verification, growth and development assessments, and neurological behavior test were conducted. Oxidative stress-related factors, miR-139-5p, HDAC4 and B-cell lymphoma 2 (Bcl-2) expression in brain tissues and serum inflammatory response were detected.
MiR-139-5p and Bcl-2 were decreased while HDAC4 was elevated in brain tissues of rats with HIBD. Growth and neurological behaviors were restrained in rats with HIBD. MiR-139-5p up-regulation or HDAC4 down-regulation alleviated pathological status, impaired oxidative stress, increased NGF and BDNF expression and inhibited neurons apoptosis of brain tissues in rats with HIBD. Increased miR-139-5p or decreased HDAC4 impaired inflammation in serum of rats with HIBD.
Our study highlights that miR-139-5p elevation or HDAC4 knockdown alleviated neurological deficit and induced neurons growth via Bcl-2 elevation.
Copyright © 2021. Published by Elsevier Inc.
microRNA-139-5p alleviates neurological deficit in hypoxic-ischemic brain damage via HDAC4 depletion and BCL-2 activation.
