Circular RNAs (circRNAs) have key roles in a variety of neurological diseases, including epilepsy. This objective of this study was to perform the functional exploration and mechanism investigation of circRNA Ubiquilin1 (circUBQLN1) in epilepsy. Epilepsy cell model was established by the treatment of Mg²⁺-free in human neurons-hippocampal (HN-h) cells. The quantitative real-time polymerase chain reaction (qRT-PCR) was used for the expression analysis of circUBQLN1, linear-UBQLN1, microRNA-155 (miR-155), and sex-determining region Y-box 7 (SOX7). Proliferation detection was completed using Cell Counting Kit-8 (CCK-8) assay. Apoptosis analysis was conducted by flow cytometry and caspase-3 assay. Oxidative stress was assessed through determining the levels of superoxide dismutase (SOD) and malondialdehyde (MDA). Target analysis was performed by dual-luciferase reporter and RNA pull-down assays. SOX7 protein level was examined by Western blot. CircUBQLN1 was downregulated in epilepsy samples and Mg²⁺-free-induced cell model. Functional analysis in vitro suggested that circUBQLN1 overexpression facilitated proliferation but reduced apoptosis and oxidative stress in Mg²⁺-free-treated HN-h cells. Target analysis showed that circUBQLN1 acted as a miR-155 sponge and miR-155-targeted SOX7. Moreover, circUBQLN1 could combine with miR-155 to regulate the SOX7 expression. Reverted assays indicated that circUBQLN1 overexpression alleviated the Mg²⁺-free-induced nerve injury by sponging miR-155, and knockdown of SOX7 abrogated the protective function of in-miR-155 or circUBQLN1 in the Mg²⁺-free-treated HN-h cells. Our data revealed that circUBQLN1 prevented nerve injury in Mg²⁺-free-treated HN-h cells by regulating the miR-155/SOX7 axis, showing that circUBQLN1 might be used as a biomolecular target for the treatment of epilepsy.

环状 RNA (circRNA) 在包括癫痫在内的多种神经系统疾病中发挥着关键作用。本研究的目的是对 circRNA Ubiquilin1 (circUBQLN1) 在癫痫中的功能探索和机制研究。^{Mg 2+}处理建立癫痫细胞模型-在人类神经元海马 (HN-h) 细胞中不含。定量实时聚合酶链反应 (qRT-PCR) 用于 circUBQLN1、linear-UBQLN1、microRNA-155 (miR-155) 和性别决定区 Y-box 7 (SOX7) 的表达分析。使用 Cell Counting Kit-8 (CCK-8) 测定完成增殖检测。通过流式细胞术和caspase-3测定进行细胞凋亡分析。通过确定超氧化物歧化酶 (SOD) 和丙二醛 (MDA) 的水平来评估氧化应激。通过双荧光素酶报告基因和 RNA 下拉分析进行目标分析。通过蛋白质印迹检查 SOX7 蛋白水平。CircUBQLN1 在癫痫样本和 Mg ^2+中下调-游离诱导的细胞模型。体外功能分析表明，circUBQLN1 过表达促进了无 Mg ²⁺处理的 HN-h 细胞的增殖，但减少了细胞凋亡和氧化应激。靶点分析表明，circUBQLN1 充当 miR-155 海绵和 miR-155 靶向 SOX7。此外，circUBQLN1 可以与 miR-155 结合来调节 SOX7 的表达。还原分析表明，circUBQLN1 过表达通过海绵化 miR-155 减轻了 Mg ²⁺诱导的神经损伤，并且 SOX7 的敲低消除了 in-miR-155 或 circUBQLN1 在无 Mg ²⁺处理的 HN-中的保护功能h 细胞。我们的数据显示，circUBQLN1 可预防 Mg ^{2+中的神经损伤}通过调节 miR-155/SOX7 轴，游离处理的 HN-h 细胞，表明 circUBQLN1 可用作治疗癫痫的生物分子靶点。