The dysregulation and regulatory mechanism of long non-coding RNA LBX2-AS1 in children with epilepsy.

BACKGROUND

Epilepsy is a long-lasting neurological condition distinguished by recurring seizures, and related to oxidative stress and inflammation. This study investigates the effects of long non-coding RNA LBX2-AS1 on childhood epilepsy.

METHODS

There were 165 epilepsy epileptic and 206 healthy children enrolled in this study. Relative LBX2-AS1, miR-873-5p, and HNRNPK expression levels were assessed using RT-PCR. Diagnostic value of LBX2-AS1 was evaluated by ROC curve. Epilepsy cell model was constructed in HT22 cells. Cell viability was assessed by CCK-8 kit. Cell apoptosis was analyzed by flow cytometer. Oxidative stress factors (SOD, GSH, LDH) and inflammatory cytokines (IL-1β, IL-6, TNF-α) were evaluated by ELISA kits. Target association was validated using dual-luciferase reporter assays. Function analysis for miR-873-5p target genes was analyzed by GO, KEGG, and PPI.

RESULTS

LBX2-AS1 was upregulated in epilepsy and had a high diagnostic value for epilepsy (AUC = 0.880, sensitivity = 80.6%, specificity = 82.0%, cutoff value = 1.14). The upregulation of LBX2-AS1 in cell model might decrease cell viability, increase apoptosis, and elevate oxidative stress and inflammation via negatively controlled miR-873-5p. Target genes of miR-873-5p were enriched in pathways related to oxidative stress, inflammation responses, and magnesium ion transmembrane transporter activity of neuronal cells. HNRNPK had the highest interaction degree with other target genes.

CONCLUSION

LBX2-AS1 is upregulated in epilepsy and is associated with increased oxidative stress, inflammation, and apoptosis via mediating miR-873-5p/HNRNPK axis in epilepsy cell model.