Background:Long noncoding RNAs have been proven to play an important role in the progression of Alzheimer’s disease (AD). However, the function of small nucleolar RNA host gene 1 (SNHG1) in AD progression remains to be studied. Objective:To explore the role of SNHG1 in AD progression and clarify its potential mechanism. Methods:Amyloid β-protein (Aβ) was used to construct an AD cell model in vitro. The expression levels of SNHG1 and miR-361-3p were determined by quantitative real-time polymerase chain reaction. Cell viability and apoptosis were measured by cell counting kit 8 assay and flow cytometry. The levels of apoptosis-related proteins and zinc finger gene 217 (ZNF217) protein were evaluated by western blot analysis. Additionally, the contents of inflammatory cytokines and oxidative stress markers were tested by enzyme-linked immunosorbent assay. Furthermore, dual-luciferase reporter and RNA immunoprecipitation assays were used to verify the interaction between miR-361-3p and SNHG1 or ZNF217. Results:Aβ could induce cell injury, while resveratrol could reverse this effect. SNHG1 expression was positively regulated by Aβ and negatively regulated by resveratrol. SNHG1 knockdown could reverse the promotion effect of Aβ on cell injury. Moreover, SNHG1 sponged miR-361-3p, and miR-361-3p targeted ZNF217. Additionally, miR-361-3p overexpression reversed the promotion effect of SNHG1 overexpression on cell injury, and ZNF217 silencing also reversed the promotion effect of miR-361-3p inhibitor on cell injury. Conclusion:SNHG1 promoted cell injury by regulating the miR-361-3p/ZNF217 axis, which might provide a theoretical basis for molecular therapy of AD.

中文翻译：

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lncRNA SNHG1敲低可通过调节海绵状miR-361-3p的ZNF217调节阿尔茨海默氏病引起的淀粉样β诱导的神经元损伤

背景：已证明长链非编码RNA在阿尔茨海默氏病（AD）的进展中起重要作用。然而，小核仁RNA宿主基因1（SNHG1）在AD进展中的功能仍有待研究。目的：探讨SNHG1在AD进展中的作用，并阐明其潜在机制。方法：采用淀粉样β蛋白（Aβ）体外构建AD细胞模型。通过定量实时聚合酶链反应确定SNHG1和miR-361-3p的表达水平。通过细胞计数试剂盒8测定和流式细胞术测量细胞活力和凋亡。通过蛋白质印迹分析评估凋亡相关蛋白和锌指基因217（ZNF217）蛋白的水平。另外，用酶联免疫吸附法检测炎症细胞因子和氧化应激标志物的含量。此外，使用双重荧光素酶报告基因和RNA免疫沉淀测定法来验证miR-361-3p与SNHG1或ZNF217之间的相互作用。结果：Aβ可诱导细胞损伤，而白藜芦醇可逆转此作用。SNHG1的表达受到Aβ的正调控，而白藜芦醇的负调控。SNHG1敲低可以逆转Aβ对细胞损伤的促进作用。此外，SNHG1使miR-361-3p和miR-361-3p靶向ZNF217。此外，miR-361-3p过表达逆转了SNHG1过表达对细胞损伤的促进作用，而ZNF217沉默也逆转了miR-361-3p抑制剂对细胞损伤的促进作用。结论：