miR-98-5p Prevents Hippocampal Neurons from Oxidative Stress and Apoptosis by Targeting STAT3 in Epilepsy in vitro

We shed lights on a pivotal mechanism of miR-98-5p in regulating neuron oxidative stress and apoptosis after seizures, providing potential biomarkers for the diagnosis of epilepsy and therapeutic targets for the treatment of epilepsy.

Magnesium ion (Mg2+)-free solution was used to establish the in vitro epilepsy model in hippocampal neurons. Oxidative stress was exhibited by measuring malondialdehyde (MDA) level and superoxide Dismutase (SOD) activity using enzyme-linked immune sorbent assay (ELISA) kits. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry were applied for the examination of neuron viability and apoptosis, respectively. Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blot were used to evaluate the mRNA and protein levels of miR-98-5p and signal transducer and activator of transcription (STAT3), respectively. The relationship between miR-98-5p and STAT3 was predicted by TargetScan 7.2, and identified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay.

Epilepsy is a serious mental disease, for which oxidative stress and hippocampal neuron death after seizure is crucial. Numerous miRNAs are involved in epilepsy. However, the function of miR-98-5p in oxidative stress and hippocampal neuron death after seizure is unclear, which is the purpose of current study.

miR-98-5p was decreased in the in vitro epileptic model of hippocampal neurons induced by Mg2+-free solution, whose overexpression rescued oxidative stress and neuron apoptosis in epileptic model. Moreover, overexpression of STAT3, one downstream target of miR-98-5p, partially eliminated the effects of miR-98-5p mimic.