Inhibition of miR-222-3p Alleviates Acute Pancreatitis by Negatively Regulating the Expression of SIRT1

IF 2.2 4区 医学 Q4 IMMUNOLOGY
Apmis Pub Date : 2025-07-04 DOI:10.1111/apm.70043
Tao Zhang, Jing Xiao, Wenzhao Chen
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引用次数: 0

Abstract

The aim of this study is to explore the correlation between the levels of miR-222-3p and the onset of acute pancreatitis (AP) and further verify the role of miR-222-3p in the pathogenesis of AP through targeted regulation of Sirtuin 1 (SIRT1). This study encompassed a total of 160 AP patients, including 80 patients with mild and moderate AP (non-SAP) and 80 patients with severe AP (SAP). The levels of miR-222-3p and SIRT1 were detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR) technology, and the potential significance of miR-222-3p in the diagnosis of AP was evaluated by receiver operating characteristic curve. The proliferation activity of cerulein-induced HPDE6-C7 cells was investigated by Cell Counting Kit-8 method. Meanwhile, the changes in the levels of inflammatory factors were quantified using enzyme-linked immunosorbent assay (ELISA) kits. The result showed that miR-222-3p was elevated in AP patients, especially in SAP patients. Elevated miR-222-3p levels showed diagnostic significance for AP. Inhibiting miR-222-3p promoted the proliferation of cerulein-damaged HPDE6-C7 cells and reduced inflammatory factor increases induced by cerulein. SIRT1 inhibition reversed the effects of miR-222-3p on cerulein-induced HPDE6-C7 cells. Inhibition of miR-222-3p may alleviate the development of AP by targeting SIRT1.

抑制miR-222-3p通过负性调节SIRT1的表达缓解急性胰腺炎
本研究旨在探讨miR-222-3p水平与急性胰腺炎(AP)发病的相关性,并通过靶向调节Sirtuin 1 (SIRT1)进一步验证miR-222-3p在AP发病机制中的作用。本研究共纳入160例AP患者,其中80例为轻中度AP(非SAP), 80例为重度AP (SAP)。采用逆转录定量聚合酶链反应(RT-qPCR)技术检测miR-222-3p和SIRT1水平,并通过受试者工作特征曲线评价miR-222-3p在AP诊断中的潜在意义。采用细胞计数试剂盒-8法检测蜡蛋白诱导的HPDE6-C7细胞的增殖活性。同时,采用酶联免疫吸附测定(ELISA)试剂盒定量测定炎症因子水平的变化。结果显示,miR-222-3p在AP患者中升高,尤其是在SAP患者中。miR-222-3p水平升高对AP具有诊断意义。抑制miR-222-3p可促进cerulein损伤的HPDE6-C7细胞增殖,降低cerulein诱导的炎症因子升高。SIRT1抑制逆转了miR-222-3p对蜡蛋白诱导的HPDE6-C7细胞的作用。抑制miR-222-3p可能通过靶向SIRT1来缓解AP的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Apmis
Apmis 医学-病理学
CiteScore
5.20
自引率
0.00%
发文量
91
审稿时长
2 months
期刊介绍: APMIS, formerly Acta Pathologica, Microbiologica et Immunologica Scandinavica, has been published since 1924 by the Scandinavian Societies for Medical Microbiology and Pathology as a non-profit-making scientific journal.
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