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Dexmedetomidine attenuates lipopolysaccharide induced acute lung injury by targeting NLRP3 via miR‐381

机译:Dexmedetomidine通过MiR-381靶向NLRP3来衰减脂多糖诱导的急性肺损伤

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Abstract Dexmedetomidine (Dex) is an agonist of α2‐adrenergic receptors, and it is used as an anxiety reducing, sedative, and pain medication in clinical. Studies have shown that dexmedetomidine protects against lipopolysaccharide (LPS)‐induced acute lung injury; however, the underlying mechanism is still unclear. To investigate, an acute lung injury mouse model was induced by intraperitoneal injection of LPS. Histopathological changes were determined by hematoxylin and eosin staining. Enzyme‐linked immunosorbent assay was used to detect cytokines in serum. microRNA expression levels were detected by quantitative reverse transcription polymerase chain reaction. Protein levels were detected by western blot. Dex treatment significantly attenuated lung injury and inhibited the expression levels of the inflammation factors via reducing the level of NACHT, LRR, and PYD domains‐containing protein 3 (NLRP3) and autocleavage of caspase‐1. Moreover, mmu‐miR‐381, which targets the mRNA of NLRP3, was upregulated after Dex treatment. Dex attenuates LPS‐induced acute lung injury via miR‐381‐targeted NLRP3.
机译:摘要Dexmedetomidine(DEX)是α2-肾上腺素能受体的激动剂,它被用作临床上的焦虑,镇静和止痛药。研究表明,德森梅蒂咪啶保护脂多糖(LPS)诱导急性肺损伤;但是,潜在的机制仍然不清楚。为了研究,通过腹腔注射LPS诱导急性肺损伤小鼠模型。通过苏木精和曙红染色测定组织病理学变化。酶联免疫吸附测定用于检测血清中的细胞因子。通过定量逆转录聚合酶链反应检测微稻草表达水平。蛋白质印迹检测蛋白质水平。 DEX治疗明显减弱肺损伤,并通过降低含NACHT,LRR和PYD域的蛋白3(NLRP3)和Caspase-1的自闭症的水平来抑制炎症因子的表达水平。此外,靶向NLRP3的mRNA的MMU-miR-381在DEX处理后上调。 DEX通过miR-381靶向NLRP3衰减LPS诱导的急性肺损伤。

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