MiR-181b suppresses the progression of epilepsy by regulation of lncRNA ZNF883.

BACKGROUND Epilepsy (EP) is a very dangerous neurological disease. MiR-181b was reported to play a regulatory role during the progression of EP. However, the mechanism by which miR-181b regulates the process of EP remains unclear. METHODS Hippocampal neurons were extracted from rats, which were treated with magnesium-free to mimic EP in vitro. CCK-8 assay was performed to test the cell viability. Gene and protein expressions in hippocampal neurons were detected by qRT-PCR, immunofluorescence and western blot, respectively. In addition, TUNEL staining was performed to test the cell apoptosis. Finally, dual luciferase report assay was used to verify the relation between miR-181b, ZNF883 and RASSF1A. RESULTS Magnesium-free significantly inhibited the proliferation of hippocampal neurons, which was reversed by miR-181b mimics. In consistent, magnesium-free induced apoptosis of cells was notably inhibited by miR-181b mimics. In addition, miR-181b suppressed the progression of EP via directly targeting RASSF1A and activating PI3K/Akt signaling. Finally, upregulation of miR-181b notably suppressed the progression of EP via regulation of ZNF883. CONCLUSION MiR-181b suppressed the progression of epilepsy via regulation of RASSF1A and lncRNA ZNF883. Thus, miR-181b might serve as a new target for treatment of EP.