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MiR-146b protects against the inflammation injury in pediatric pneumonia through MyD88/NF-κB signaling pathway.

MiR-146b通过MyD88/NF-κ b信号通路保护小儿肺炎的炎症损伤。

  • 影响因子:1.61
  • DOI:10.1080/23744235.2019.1671987
  • 作者列表:"Zhang L","Dong L","Tang Y","Li M","Zhang M
  • 发表时间:2020-01-01
Abstract

:Background: Pneumonia is a common respiratory disease worldwide that can be prevented and treated. However, it is considered to be the leading cause of children death. The present study was aimed to explore the functional role and molecular mechanism of miR-146b in the inflammation injury in pediatric pneumonia.Materials and methods: The lipopolysaccharide (LPS)-induced pulmonary injury cell model was established in WI-38 human lung fibroblasts cells. QRT-PCR and Western blot was applied to detect miR-146b and MyD88 expression. ELISA assay was used to analyze the production of pro-inflammatory factors. Cell viability was evaluated by CCK-8 assay. The apoptosis proteins and the downstream genes of NF-κB pathway were detected by Western blot.Results: we displayed that miR-146b was down-regulated, whereas MyD88 was up-regulated in the serum of children patients with pneumonia and in WI-38 cells treated with LPS. Moreover, re-expression of miR-146b suppressed the production of inflammatory factors in the serum of pneumonia patients and WI-38 cells treated with LPS. In addition, elevating miR-146b expression increased WI-38 cell viability and reduced cell apoptosis. More importantly, bioinformatics analysis revealed that MyD88 was a target of miR-146b and could overturn the protective effect of miR-146b on the inflammation injury in LPS-injured WI-38 cells. Furthermore, miR-146b over-expression inhibited the activation of NF-κB signaling pathway by suppressing MyD88.Conclusion: miR-146b attenuated the inflammation injury in pediatric pneumonia through inhibiting MyD88/NF-κB signaling pathway. These preliminarily findings further deepened our understanding of this mechanism and identified new potential therapeutic targets for pediatric pneumonia.

摘要

背景: 肺炎是世界范围内常见的可预防和治疗的呼吸系统疾病。然而,它被认为是儿童死亡的主要原因。本研究旨在探讨miR-146b在小儿肺炎炎症损伤中的作用及分子机制。材料与方法: 建立人肺成纤维细胞脂多糖 (LPS) 诱导WI-38 肺损伤模型。应用QRT-PCR和Western blot检测miR-146b和MyD88 的表达。ELISA法分析促炎因子的产生。通过CCK-8 试验评价细胞活力。Western blot检测细胞凋亡蛋白及NF-κ b通路下游基因。结果: 显示miR-146b表达下调,而MyD88 上调血清患儿肺炎和WI-38 细胞脂多糖 (LPS).此外,miR-146b的重新表达抑制了肺炎患者血清和LPS处理WI-38 细胞中炎症因子的产生。此外,提高miR-146b表达增加WI-38 细胞活力和减少细胞凋亡。更重要的是,生物信息学分析发现MyD88 是miR-146b的靶点,可以推翻miR-146b对LPS损伤WI-38 细胞炎症损伤的保护作用。此外,miR-146b过表达通过抑制MyD88 抑制NF-κ b信号通路的激活。结论: miR-146b通过抑制MyD88/NF-κ b信号通路减轻小儿肺炎的炎症损伤。这些初步发现进一步加深了我们对这一机制的理解,并确定了小儿肺炎新的潜在治疗靶点。

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翻译标题与摘要 下载文献
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发表时间:2020-04-01
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DOI:10.1007/s15010-020-01401-y
作者列表:["Cheng ZJ","Shan J"]

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呼吸道感染方向

呼吸道感染分为上呼吸道感染与下呼吸道感染。上呼吸道感染是指自鼻腔至喉部之间的急性炎症的总称,是最常见的感染性疾病。下呼吸道感染是最常见的感染性疾患,治疗时必须明确引起感染的病原体以选择有效的抗生素。

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