MiR-128 is upregulated in epilepsy and promotes apoptosis through the SIRT1 cascade

Abstract

The present study aimed to examine the functional and molecular effects of miR-128 in epilepsy, in order to investigate its potential protective mechanisms. Firstly, miR-128 expression in rats with lithium chloride-induced epilepsy was demonstrated to be increased compared with the control rats. Subsequently, results from an in vitro epilepsy model demonstrated that overexpression of miR-128 promoted nerve cell apoptosis, increased the protein expression of tumor protein p53, BCL2 associated X (Bax) and Cytochrome c, and enhanced caspase-3/9 activity, whereas it suppressed the protein expression of sirtuin 1 (SIRT1). In addition, these alterations may be reversed by the downregulation of miR-128. Furthermore, treatment with CAY10602, a SIRT1 agonist, reduced the effects of miR-128 on nerve cells in vitro. Treatment with pifithrin-β hydrobromide, a p53 inhibitor, was additionally able to mitigate the effects of miR-128 in vitro. In conclusion, the present findings indicated that anti-miR-128 may exert neuroprotective effects in epilepsy, through the SIRT1/p53/Bax/Cytochrome c/caspase signaling pathway.