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首页> 外文期刊>Journal of biochemical and molecular toxicology >LncRNASnhg8 attenuates microglial inflammation response and blood-brain barrier damage in ischemic stroke through regulating miR-425-5p mediated SIRT1/NF-κB signaling
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LncRNASnhg8 attenuates microglial inflammation response and blood-brain barrier damage in ischemic stroke through regulating miR-425-5p mediated SIRT1/NF-κB signaling

机译：通过调节miR-425-5p介导的SIRT1 / NF-κB信号传导，LNCRNASNHG8衰减缺血性卒中中的微胶质炎症反应和血脑屏障损伤

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摘要

Increasing studies have indicated that abnormal expressed long noncoding RNAs (lncRNAs) play a vital role in ischemic stroke. Small nucleolar RNA host gene 8 (Snhg8), a member of lncRNAs, has been found to induce neuronal apoptosis in chronic cerebral ischemia models. Here, we aim to explore the function and molecular mechanism of Snhg8 in modulating microglial inflammation as well as brain microvascular endothelial cell (BMEC) damage following ischemic injury. Our data suggested that Snhg8 was low-expressed in the brain tissues of mice that underwent middle cerebral artery occlusion (MCAO) surgery and oxygen-glucose deprivation (OGD)-treated primary microglia and BMECs. Gain- or loss-of function approaches found that Snhg8 upregulation not only attenuated ischemic induced inflammatory response in microglia but also relieved BMECs injury both in vitro and in vivo. Furthermore, we conducted a bioinformatics analysis to explore the underlying mechanism of Snhg8. The results indicated that Snhg8 served as a competitive endogenous RNA by sponging miR-425-5p, which was proved to promote microglial inflammation and BMECs injury by targeting sirtuin1 (SIRT1)-mediated nuclear factor-κB (NF-κB) pathway. Overall, these results revealed that the Snhg8/miR-425-5p/SIRT1/NF-κB axis plays a critical role in the regulation of cerebral ischemia-induced microglial inflammation and brain-blood barrier damage.
机译：越来越多的研究表明，异常表达的长非编码RNA（lncRNAs）在缺血性中风中起着至关重要的作用。小核仁RNA宿主基因8（Snhg8）是lncRNAs的一个成员，在慢性脑缺血模型中可诱导神经元凋亡。在此，我们旨在探讨Snhg8在缺血性损伤后调节小胶质细胞炎症和脑微血管内皮细胞（BMEC）损伤中的功能和分子机制。我们的数据表明，在接受大脑中动脉闭塞（MCAO）手术和氧糖剥夺（OGD）治疗的小鼠原代小胶质细胞和BMEC的脑组织中，Snhg8表达较低。功能获得或功能丧失的研究发现，Snhg8上调不仅可以减轻缺血诱导的小胶质细胞炎症反应，而且可以减轻体外和体内的BMECs损伤。此外，我们还进行了生物信息学分析，以探索Snhg8的潜在机制。结果表明，Snhg8通过吸附miR-425-5p作为一种竞争性内源性RNA，通过靶向sirtuin（SIRT1）介导的核因子-κB（NF-κB）途径，证明其促进小胶质细胞炎症和BMECs损伤。总的来说，这些结果表明Snhg8/miR-425-5p/SIRT1/NF-κB轴在脑缺血诱导的小胶质细胞炎症和脑血屏障损伤的调节中起着关键作用。

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