Abstract
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.
Highlights
Epilepsy (Ep) is a chronic brain disorder characterized by recurrent episodes caused by the excessive discharge of a certain part of the neuron group in the brain [1]
Further studying the mechanism of miR-136 affecting temporal lobe epilepsy (TLE), the results showed that the levels of Wnt/β-catenin signaling pathway-related proteins β-catenin, Cyclin D1, and c-myc in the hippocampus tissue of the Ep group were significantly higher than those in the control group, while the β-catenin, Cyclin D1, and c-myc in the hippocampus tissue were significantly reduced after overexpression of miR-136
TLE is the most common type of focal epilepsy, with seizures beginning in the temporal lobe structure [22]
Summary
To explore the effect of miR-136 on temporal lobe epilepsy (Ep) and its mechanism of action. The expression of miR-136 in the hippocampus tissue was detected by qRT-PCR. 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. 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. Overexpression of miR-136 significantly reduced the apoptosis rate in the hippocampus tissue and inhibited the levels of inflammatory factors. MiR-136 downregulates the expression of Wnt/β-catenin signaling pathway-related proteins. MiR-136 could exert its neuroprotective influence on temporal lobe epilepsy rats by inhibiting the Wnt/β-catenin signaling pathway Conclusion. miR-136 could exert its neuroprotective influence on temporal lobe epilepsy rats by inhibiting the Wnt/β-catenin signaling pathway
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