MiR-128-3p inhibits the inflammation by targeting MAPK6 in penicillin-induced astrocytes

Abstract

Objective Epilepsy causes physical and mental damage to patients. As well known, microRNAs (miRNAs) provide therapeutic target potentials for patients with epilepsy. miR-128-3p was previously reported to be downregulated in temporal lobe epilepsy (TLE) patients, however, its detailed function in epilepsy is unknown. Methods Astrocytes function in epilepsy, penicillin-induced astrocytes can be used as a model for seizures in vitro. Currently, the expression levels of mitogen-Activated protein kinase 6 (MAPK6), interleukin-1 beta (IL-1β) and tumor necrosis factor-Alpha (TNF-α) were determined by western blot and reverse transcription-quantitative PCR analyses (RT-qPCR). The expression level of miR-128-3p was evaluated by RT-qPCR. TargetScan 7.1 and dual luciferase reporter assay were used for prediction and verification of interaction between miR-128-3p and MAPK6 3′ untranslated region (UTR). Cell viability was detected by 3-(4,5-dimethyl-2-Thiazolyl)-2,5-diphenyl-2-H-Tetrazolium bromide (MTT) assay. Results We found that penicillin-induced decrease in cell viability, and increase of TNF-α/IL-1β in primary astrocytes. There were lower miR-128-3p and higher MAPK6 in penicillin-Treated primary astrocytes. miR-128-3p overexpression rescued penicillin-induced reduction of cell viability, and upregulation of TNF-α/IL-1β, which was partially abolished by MAPK6 overexpression. Conclusion Altogether, miR-128-3p attenuates penicillin-induced cell injury and inflammation in astrocytes by targeting MAPK6, thus providing a protective role in epilepsy.