Acute kidney injury (AKI) is a common organ injury in sepsis, which leads to poor prognosis. Long noncoding RNA (lncRNA) small nucleolus RNA host gene 14 (SNHG14) was recognized to induce cell injury in LPS-induced acute lung injury and Parkinson’s disease. We want to investigate the functions and mechanisms of SNHG14 in sepsis-induced AKI. Increased expression of SNHG14 was observed in LPS-induced HK-2 cells, and this was due to the activation of the TLR4/NF-κB pathway. In vitro studies showed that SNHG14 was involved in the oxidative stress, inflammation, and apoptosis of LPS-induced HK-2 cells. Further investigations confirmed that SNHG14 exerted the functions via miR-93 which could regulate the activation of NF-κB and STAT3 signaling by targeting IRAK4 and IL-6R. We also found that silencing SNHG14 also alleviated cellular injury processes of IL-1β and IL-6 in HK-2 cells via miR-93. We demonstrate that SNHG14 accelerates cellular injury in sepsis-induced AKI by activating IRAK4/NF-κB and IL-6R/STAT3 signaling via miR-93.

中文翻译：

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lncRNA SNHG14通过调节miR-93在脓毒症诱导的急性肾损伤中发挥作用

急性肾损伤（AKI）是脓毒症中常见的器官损伤，预后较差。长链非编码 RNA (lncRNA) 小核仁 RNA 宿主基因 14 (SNHG14) 被认为在 LPS 诱导的急性肺损伤和帕金森病中诱导细胞损伤。我们想研究 SNHG14 在败血症诱导的 AKI 中的功能和机制。在LPS诱导的HK-2细胞中观察到SNHG14的表达增加，这是由于TLR4 / NF-的活化κ乙通路。体外研究表明，SNHG14 参与 LPS 诱导的 HK-2 细胞的氧化应激、炎症和凋亡。进一步研究证实SNHG14通过miR-93发挥调节NF- κ活化的功能B 和 STAT3 信号通过靶向 IRAK4 和 IL-6R。我们还发现沉默 SNHG14 还通过 miR-93减轻了 HK-2 细胞中 IL-1 β和 IL-6 的细胞损伤过程。我们证明，SNHG14通过激活IRAK4 / NF-加速脓毒症诱导的AKI的细胞损伤κ经由的miR-93 B和IL-6R / STAT3信号传导。