Aim

Acute lung injury (ALI) is the mild form of acute respiratory distress syndrome (ARDS) which is a common lung disease with a high incidence and mortality rate. Recent studies manifested that some circular RNAs were associated with ALI. In this study, we aimed to uncover the effect of circular RNA circ_0054633 on ALI initiation and progression and proposed a new mechanism related to ALI.

Methods

The lipopolysaccharides (LPS)-induced acute lung injury model were build both in vivo of rat and in vitro of primary murine pulmonary microvascular endothelial cells (MPVECs). Hematoxylin and eosin (H&E) was employed to observe the tissue morphology and estimate the degree of lung damage. We used real-time quantitative polymerase chain reaction (RT-qPCR) to measure the expression level of circ_0054633. The expression levels of inflammatory cytokines IL-17A and tumor necrosis factor-α (TNF-α) were detected by ELISA. The effects of circ_0054633 on MPVECs proliferation and apoptosis were detected with the help of CCK-8 and apoptosis assay, separately. The expression level of NF-κB p65 protein was measured by Western blot.

Results

circ_0054633, IL-17A, TNF-α and NF-κB p65 were all overexpressed in LPS-treated rat and MPVECs, and LPS enhanced the proliferation and apoptosis of MPVECs. While circ_0054633 silencing reversed the above promotion effects of LPS on IL-17A, TNF-α expression and MPVECs proliferation and apoptosis.

Conclusions

Quietness of circ_0054633 alleviated LPS-induced ALI via NF-κB signaling pathway, implicating circ_0054633 may be a potential biomarker for diagnose and therapy of ALI.

中文翻译：

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环状RNA circ_0054633的安静性通过NF-κB信号通路减轻了脂多糖诱导的急性肺损伤模型的炎症和增殖。

目标

急性肺损伤（ALI）是急性呼吸窘迫综合征（ARDS）的一种轻度形式，是一种常见的肺部疾病，发病率和死亡率很高。最近的研究表明，某些环状RNA与ALI相关。在这项研究中，我们旨在揭示环状RNA circ_0054633对ALI起始和进展的影响，并提出了一种与ALI相关的新机制。

方法

脂多糖（LPS）诱导的急性肺损伤模型是在大鼠体内和体外建立原代鼠肺微血管内皮细胞（MPVEC）的。使用苏木精和曙红（H＆E）观察组织形态并评估肺损伤程度。我们使用实时定量聚合酶链反应（RT-qPCR）来测量circ_0054633的表达水平。ELISA法检测炎症细胞因子IL-17A和肿瘤坏死因子-α（TNF-α）的表达水平。分别通过CCK-8和凋亡测定法检测circ_0054633对MPVECs增殖和凋亡的影响。Western blot检测NF-κBp65蛋白的表达水平。

结果

circ_0054633，IL-17A，TNF-α和NF-κBp65在LPS处理的大鼠和MPVEC中均过表达，LPS增强MPVEC的增殖和凋亡。circ_0054633沉默逆转了LPS对IL-17A，TNF-α表达以及MPVEC增殖和凋亡的上述促进作用。

结论

circ_0054633的安静通过NF-κB信号通路减轻了LPS诱导的ALI，提示circ_0054633可能是诊断和治疗ALI的潜在生物标志物。