Epileptic disorders : international epilepsy journal with videotape · 2026
The SNHG16/miR-485-5p axis exacerbates neuronal injury in pediatric temporal lobe epilepsy.
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Ding Xuemin, Luo Haixia
Аннотация
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.
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.