The Neuroprotective Effect of miR-136 on Pilocarpine-Induced Temporal Lobe Epilepsy Rats by Inhibiting Wnt/β-Catenin Signaling Pathway

OBJECTIVE: To explore the effect of miR-136 on temporal lobe epilepsy (Ep) and its mechanism of action. METHODS: 30 male rats were injected intraperitoneally with 30 mg/kg pilocarpine to construct a rat temporal lobe epilepsy model, and they were randomly divided into 5 groups (n = 6 per group): control group, Ep group, agomir NC group, miR-136 agomir group, and miR-136+LiCl group. The brain tissues of the rats were collected 7 days after the treatment. The expression of miR-136 in the hippocampus tissue was detected by qRT-PCR. H&E and Nissl staining were used to observe the histopathological changes and neuron damage in the hippocampus tissue. IL-1β, IL-6, and TNF-α levels in the hippocampus tissue were detected by ELISA. Flow cytometry was used to detect the apoptosis rate in the hippocampus tissue. Western blot was used to detect the expression levels of c-Caspase-3, Bcl-2, β-catenin, Cyclin D1, and c-myc protein in the hippocampus. RESULTS: The expression of miR-136 was significantly downregulated in the hippocampus tissue of epileptic rats. After overexpression of miR-136, the number of seizures and the duration of epilepsy in rats were significantly reduced. At the same time, hippocampal tissue damage was improved considerably, and the degree of neuronal damage decreased. Overexpression of miR-136 also significantly reduced the apoptosis rate in the hippocampus tissue and inhibited the levels of inflammatory factors. Meanwhile, miR-136 downregulates the expression of Wnt/β-catenin signaling pathway-related proteins. However, Wnt pathway activator LiCl could destroy the protective effect of miR-136. CONCLUSION: miR-136 could exert its neuroprotective influence on temporal lobe epilepsy rats by inhibiting the Wnt/β-catenin signaling pathway.