The SNHG16/miR-485-5p axis exacerbates neuronal injury in pediatric temporal lobe epilepsy.
TL;DR
SNHG16 is highly expressed in pediatric TLE and has certain diagnostic potential and exacerbates epilepsy-related neuronal damage by binding to and suppressing miR-485-5p function, which provides novel insights into understanding the disease mechanism.
Abstract
Objective
This study aims to investigate the expression pattern of long noncoding RNA SNHG16 in pediatric temporal lobe epilepsy (TLE), its clinical diagnostic value, and its molecular mechanisms in epilepsy-related neuronal damage.
Methods
This study included 78 newly diagnosed pediatric TLE patients and 75 healthy control children. SNHG16 expression was detected via RT-qPCR, and its diagnostic efficacy was evaluated using ROC curves. In vitro, a TLE model was established in human hippocampal neuronal cells treated with magnesium-free medium. Cell viability, apoptosis, inflammatory factor levels (IL-6, IL-1β, TNF-α), and oxidative stress markers (SOD, GSH, MDA) were assessed using MTT assay, flow cytometry, ELISA, and biochemical kits, respectively. The targeting relationship between SNHG16 and miR-485-5p was validated through dual-luciferase reporter assays and RIP experiments.
Results
Serum SNHG16 expression was significantly upregulated in TLE pediatric patients, with an area under the curve (AUC) of 0.895. In cell models, silencing SNHG16 significantly alleviated magnesium-deprivation-induced decreases in cell viability, increased apoptosis, oxidative stress, and inflammatory responses. Mechanistically, SNHG16 directly binds and negatively regulates miR-485-5p expression in the cytoplasm. Inhibiting miR-485-5p reversed the neuroprotective effects induced by SNHG16 knockdown.
Conclusion
SNHG16 is highly expressed in pediatric TLE and has certain diagnostic potential. It exacerbates epilepsy-related neuronal damage by binding to and suppressing miR-485-5p function. This study provides novel insights into understanding the disease mechanism.