Introduction: Long noncoding RNA small nuclear host gene 1 (SNHG1) was involved in neuroinflammation in microglial BV-2 cells; however, its interaction with microRNA (miR)-181b in lipopolysaccharide (LPS)-induced BV-2 cells remained poor. Methods: BV-2 cells were treated with LPS and then were subjected to observation on morphology and immunofluorescence staining. After transfection, levels of inflammatory cytokines interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) were determined with enzyme-linked immunosorbent assay (ELISA). The potential binding sites between SNHG1 and miR-181b were confirmed using dual-luciferase reporter assay. Quantitative real-time polymerase chain reaction and Western blot were applied for detecting the mRNA and protein expressions of proinflammatory cytokines, ionized calcium-binding adapter molecule 1 (Iba1), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). Results: LPS led to the morphological changes and activation of BV-2 cells. The transfection of SNHG1 overexpression vector further promoted LPS-induced SNHG1 upregulation, inflammatory cytokines (IL-1β, IL-6, and TNF-α) generation and Iba-1, COX-2, and iNOS expressions, whereas silencing SNHG1 did the opposite. miR-181b functions as a downstream miRNA of SNHG1. In LPS-treated cells, the inhibition of miR-181b induced by SNHG1 promoted inflammation response and the expressions of Iba-1, COX-2, and iNOS. Conclusion: SNHG1 was involved in LPS-induced microglial activation and inflammation response via targeting miR-181b, providing another evidence of the roles of SNHG1 implicated in neuroinflammation of microglia.
Neuroimmunomodulation

中文翻译：

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长非编码 RNA SNHG1 通过靶向 miR-181b 促进脂多糖诱导的小胶质细胞激活和炎症


简介：长非编码RNA小核宿主基因1（SNHG1）参与小胶质细胞BV-2细胞的神经炎症；然而，在脂多糖（LPS）诱导的 BV-2 细胞中，其与 microRNA（miR）-181b 的相互作用仍然很差。方法：用LPS处理BV-2细胞，进行形态学和免疫荧光染色观察。转染后，通过酶联免疫吸附测定（ELISA）测定炎症细胞因子白细胞介素-1β（IL-1β）、IL-6和肿瘤坏死因子-α（TNF-α）的水平。使用双荧光素酶报告基因测定证实了 SNHG1 和 miR-181b 之间的潜在结合位点。采用实时定量聚合酶链反应和Western blot检测促炎细胞因子、离子钙结合接头分子1（Iba1）、环氧合酶-2（COX-2）、诱导型一氧化氮合酶（iNOS）的mRNA和蛋白表达。 ）。结果： LPS导致BV-2细胞形态改变和活化。 SNHG1过表达载体的转染进一步促进LPS诱导的SNHG1上调、炎症细胞因子（IL-1β、IL-6和TNF-α）的产生以及Iba-1、COX-2和iNOS的表达，而沉默SNHG1则相反。 miR-181b 作为 SNHG1 的下游 miRNA。在 LPS 处理的细胞中，SNHG1 诱导的 miR-181b 抑制促进了炎症反应以及 Iba-1、COX-2 和 iNOS 的表达。结论： SNHG1通过靶向miR-181b参与LPS诱导的小胶质细胞活化和炎症反应，为SNHG1在小胶质细胞神经炎症中的作用提供了另一个证据。
 神经免疫调节