Antagonist targeting microRNA-146a protects against lithium-pilocarpine-induced status epilepticus in rats by nuclear factor-κB pathway.

Previous studies have indicated that nuclear factor-κB (NF-κB) has an important role in the pathogenesis of epilepsy. The aim of the present study was to evaluate the expression of microRNA (miRNA)‑146a, phosphorylated (p)‑P65/P65, B‑cell lymphoma‑2(Bcl‑2)/Bcl‑2‑associated X protein (Bax) and pro‑inflammatory cytokines, such as interleukin (IL)‑6, IL‑1β and tumor necrosis factor (TNF‑α) in the brain tissue of rats with epilepsy. Sprague‑Dawley rats were used to establish the epilepsy model using the lithium‑pilocarpine method. The expression of miR‑146a, pro‑inflammatory cytokines, P‑glycoprotein (P‑gp), Bcl‑2/Bax and p‑P65/P65 were assessed by reverse transcription‑semi‑quantitative polymerase chain reaction, enzyme‑linked immunosorbent assay and western blotting, respectively. Hematoxylin and eosin staining was used to determine the pathology of epilepsy. The current findings revealed that the expression of miR‑146a was greater in the model group compared with the control group, and that the expression of miR‑146a reached a maximum at 7 days post‑treatment. The expression levels of IL‑1β, IL‑6 and TNF‑α were significantly reduced in the miR‑146a antagonist group when compared with the model group. Additionally, the expression levels of P‑gp and p‑P65/P65 were significantly reduced following the addition of the miR‑146a antagonist, whereas the expression levels of Bcl‑2/Bax significantly increased under the same conditions. Therefore, the NF‑κB pathway and miR‑146a may be potential therapeutic targets in the treatment of epilepsy.