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miR-193a-5p 和 miR-320-5p 对胆酸钠诱导的 AR42J 细胞损伤的保护作用。

Protective Effect of miR-193a-5p and miR-320-5p on Caerulein-Induced Injury in AR42J Cells.

机构信息

Department of Intensive Care Unit, Dongying District People's Hospital, Dongying City, Shandong Province, People's Republic of China.

Department of Emergency, Shengli Oilfield Central Hospital, Dongying City, Shandong Province, People's Republic of China.

出版信息

Dig Dis Sci. 2021 Dec;66(12):4333-4343. doi: 10.1007/s10620-020-06800-7. Epub 2021 Jan 6.

DOI:10.1007/s10620-020-06800-7
PMID:33405047
Abstract

BACKGROUND

Acute pancreatitis is a common inflammatory disease. MicroRNAs have been implicated in the pathogenesis of acute pancreatitis.

AIMS

The purpose of this study was to investigate the precise roles of miR-193a-5p and miR-320-5p in AP.

METHODS

The levels of miR-193a-5p, miR-320-5p and tumor necrosis factor receptor-associated factor 3 were detected by quantitative real-time polymerase chain reaction. Cell apoptosis was determined using flow cytometry. Enzyme-linked immunosorbent assay was performed to measure TNF-α, IL-6, IL-1β and IL-8 production, amylase activity, and malondialdehyde content. Targeted relationship between miR-193a-5p or miR-320-5p and TRAF3 was confirmed by the dual-luciferase reporter and RNA immunoprecipitation assays.

RESULTS

Our data showed that miR-193a-5p and miR-320-5p were down-regulated in acute pancreatitis serum and caerulein-treated AR42J cells. The increased expression of miR-193a-5p or miR-320-5p alleviated caerulein-induced cell injury in AR42J cells. Tumor necrosis factor receptor-associated factor 3 was a direct target of miR-193a-5p and miR-320-5p in AR42J cells. Moreover, miR-193a-5p and miR-320-5p regulated caerulein-induced AR42J cells injury through targeting tumor necrosis factor receptor-associated factor 3.

CONCLUSION

The present findings demonstrated that miR-193a-5p and miR-320-5p protected AR42J cells against caerulein-induced cell injury by targeting tumor necrosis factor receptor-associated factor 3, highlighting their roles as potential therapeutic targets for acute pancreatitis treatment.

摘要

背景

急性胰腺炎是一种常见的炎症性疾病。微小 RNA(miRNA)已被认为与急性胰腺炎的发病机制有关。

目的

本研究旨在探讨 miR-193a-5p 和 miR-320-5p 在急性胰腺炎(AP)中的精确作用。

方法

通过实时定量聚合酶链反应检测 miR-193a-5p、miR-320-5p 和肿瘤坏死因子受体相关因子 3 的水平。通过流式细胞术测定细胞凋亡。酶联免疫吸附试验测定 TNF-α、IL-6、IL-1β 和 IL-8 的产生、淀粉酶活性和丙二醛含量。通过双荧光素酶报告和 RNA 免疫沉淀试验证实 miR-193a-5p 或 miR-320-5p 与 TRAF3 之间的靶向关系。

结果

我们的数据显示,miR-193a-5p 和 miR-320-5p 在急性胰腺炎血清和蛙皮素处理的 AR42J 细胞中下调。miR-193a-5p 或 miR-320-5p 的表达增加缓解了蛙皮素诱导的 AR42J 细胞损伤。肿瘤坏死因子受体相关因子 3 是 AR42J 细胞中 miR-193a-5p 和 miR-320-5p 的直接靶标。此外,miR-193a-5p 和 miR-320-5p 通过靶向肿瘤坏死因子受体相关因子 3 调节蛙皮素诱导的 AR42J 细胞损伤。

结论

本研究结果表明,miR-193a-5p 和 miR-320-5p 通过靶向肿瘤坏死因子受体相关因子 3 保护 AR42J 细胞免受蛙皮素诱导的细胞损伤,强调了它们作为急性胰腺炎治疗潜在治疗靶点的作用。

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