{"title":"The miR-146a-associated HDAC2 regulation of PI3K is involved in pancreatitis in vitro","authors":"Ding-wen Zhong , Xiang-tian Zeng , Wen-hui Chen , Xian-yu Huang , Jia-xin Liu , Yong-hui Liao","doi":"10.1016/j.bbrep.2025.102057","DOIUrl":null,"url":null,"abstract":"<div><h3>Purpose</h3><div>To investigate the association between miR-146a/HDAC2 and their regulatory roles on the PI3K expression during pancreatitis.</div></div><div><h3>Methods</h3><div>Rat pancreatic AR42J cells were treated with LPS for simulating pancreatitis. Expression levels of inflammatory factors (IL-6, TNF-α) and miR-146a were d<strong>etected to</strong> determine the optimal LPS concentration for establishing an in vitro pancreatitis model<strong>.</strong> Cell proliferation and apoptosis were analyzed using CCK-8 and flow cytometry<strong>.</strong> Immunofluorescence was performed to assess co-localization of HDAC2 and PI3K. ELISA quantified TNF-α and IL-6 levels in cell supernatants. A dual-luciferase assay verified the targeting relationship between miR-146a and HDAC2.</div></div><div><h3>Results</h3><div>Compared to controls, the cell proliferation ability of the pancreatitis model group was decreased, whereas TSA and miR-146a mimic interventions restored proliferation. The expression of IL-6 and TNF-αin the LPS group was higher than that in the control group, and their expression decreases in the TSA and miR-146a mimic intervention group. Besides the dual luciferase detected the targeting relationship between miR-146a and HDAC2, the immunofluorescence showed co-localization of HDAC2 and PI3K.</div></div><div><h3>Conclusions</h3><div>TSA and miR-146a mimic enhance proliferation and reduce inflammation in pancreatitis cells. The miR-146a/HDAC2 axis may mediate therapeutic effects in pancreatitis by modulating the PI3K expression.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 102057"},"PeriodicalIF":2.3000,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochemistry and Biophysics Reports","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S240558082500144X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Purpose
To investigate the association between miR-146a/HDAC2 and their regulatory roles on the PI3K expression during pancreatitis.
Methods
Rat pancreatic AR42J cells were treated with LPS for simulating pancreatitis. Expression levels of inflammatory factors (IL-6, TNF-α) and miR-146a were detected to determine the optimal LPS concentration for establishing an in vitro pancreatitis model. Cell proliferation and apoptosis were analyzed using CCK-8 and flow cytometry. Immunofluorescence was performed to assess co-localization of HDAC2 and PI3K. ELISA quantified TNF-α and IL-6 levels in cell supernatants. A dual-luciferase assay verified the targeting relationship between miR-146a and HDAC2.
Results
Compared to controls, the cell proliferation ability of the pancreatitis model group was decreased, whereas TSA and miR-146a mimic interventions restored proliferation. The expression of IL-6 and TNF-αin the LPS group was higher than that in the control group, and their expression decreases in the TSA and miR-146a mimic intervention group. Besides the dual luciferase detected the targeting relationship between miR-146a and HDAC2, the immunofluorescence showed co-localization of HDAC2 and PI3K.
Conclusions
TSA and miR-146a mimic enhance proliferation and reduce inflammation in pancreatitis cells. The miR-146a/HDAC2 axis may mediate therapeutic effects in pancreatitis by modulating the PI3K expression.
期刊介绍:
Open access, online only, peer-reviewed international journal in the Life Sciences, established in 2014 Biochemistry and Biophysics Reports (BB Reports) publishes original research in all aspects of Biochemistry, Biophysics and related areas like Molecular and Cell Biology. BB Reports welcomes solid though more preliminary, descriptive and small scale results if they have the potential to stimulate and/or contribute to future research, leading to new insights or hypothesis. Primary criteria for acceptance is that the work is original, scientifically and technically sound and provides valuable knowledge to life sciences research. We strongly believe all results deserve to be published and documented for the advancement of science. BB Reports specifically appreciates receiving reports on: Negative results, Replication studies, Reanalysis of previous datasets.