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

• Published in: Biochemistry and cell biology Vol. 98; no. 2; pp. 208 - 218
• Main Authors: Li, Na, Yue, Linli, Wang, Jun, Wan, Zhenzhen, Bu, Wenhao
• Format: Journal Article
• Language: English
• Published: Canada NRC Research Press 01.03.2020; Canadian Science Publishing NRC Research Press
• Subjects: Anesthesia; Animals; Animals, Newborn; Antioxidants - pharmacology; Apoptosis; Attenuation; Brain; Calcium - metabolism; Calcium ions; Calcium permeability; Cell Proliferation; Cell Survival; Cyclin-dependent kinase inhibitor p27; Cyclin-Dependent Kinase Inhibitor p27 - metabolism; Genes, Reporter; Halides; Health aspects; Hippocampus; Hippocampus - drug effects; Infusions, Intraventricular; Isoflurane; Isoflurane - toxicity; kip1; Medical research; Medicine, Experimental; microARN-24; MicroRNA; microRNA-24; MicroRNAs - metabolism; Microscopy, Electron, Transmission; miRNA; Mitochondria; Mitochondria - metabolism; neurones de l’hippocampe de rat; Neurons; Neurons - drug effects; Neurons - metabolism; Neurotoxicity; Overexpression; Oxidative stress; Oxidative Stress - drug effects; p27; Permeability; rat hippocampal neurons; Rats; Rats, Sprague-Dawley; Reporter gene; Rodents; stress oxydant; Target recognition; Therapeutic applications; Viability; China; California; p27kip1; microARN-24; microRNA-24; isoflurane; neurones de l’hippocampe de rat; oxidative stress; stress oxydant; rat hippocampal neurons
• ISSN: 0829-8211; 1208-6002
• DOI: 10.1139/bcb-2019-0188

Several miRNAs have been recently suggested 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 was used to induce neurotoxicity in a rat model. Gain- and loss-of-function of miR-24 was performed, and the size and Ca 2+ permeability of mitochondria, as well as cell proliferation and apoptosis, and levels of oxidative-stress-related factors were measured both in vivo and in vitro. Dual luciferase reporter gene assays were used to identify the target relationship between miR-24 and p27 kip1 . In this study, isoflurane treatment decreased miR-24 expression, after which, levels of neuron apoptosis and oxidative-stress-related factors were elevated and neuron viability was reduced. Over-expression of miR-24 inhibited oxidative damage and neuronal apoptosis in hippocampal tissues, and suppressed the size and Ca 2+ permeability of mitochondria of hippocampal neurons. miR-24 enhanced the viability of rat hippocampal neurons by targeting p27 kip1 . To conclude, this study demonstrated that miR-24 attenuates isoflurane-induced neurotoxicity in rat hippocampus via its antioxidative properties and inhibiting p27 kip1 expression.