MicroRNA-24 alleviates isoflurane-induced neurotoxicity in rat hippocampus via attenuation of oxidative stress.

Abstract

Recently, several miRNAs have been suggested to serve as potential therapeutic targets for anesthesia-related diseases. This study was carried out to explore the biological roles of miR-24 in isoflurane-treated rat hippocampal neurons. Isoflurane-treated rat model was established to induce neurotoxicity. Gain- and loss- of function of miR-24 was performed and the size and Ca2+ permeability of mitochondria, cell proliferation and apoptosis and levels of oxidative stress-related factors were measured both in vivo and in vitro. Dual luciferase reporter gene assay was used to identify the target relation between miR-24 and p27kip1. In this study, isoflurane treatment decreased miR-24 expression, after which the neuronal apoptosis and the oxidative-stress-related factors were elevated while the neuronal viability was reduced. Over-expression of miR-24 inhibited oxidative damage and neuronal apoptosis in hippocampus and suppressed the size and Ca2+ permeability of mitochondria of hippocampal neurons. miR-24 enhanced the viability of rat hippocampal neurons by targeting p27kip1. To conclude, this study demonstrated that miR-24 could attenuate isoflurane-induced neurotoxicity in rat hippocampus via anti-oxidative stress function and inhibiting p27kip1 expression.