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Rat pancreatic exocrine cells (AR42J) were treated with caerulein to induce pancreatitis\u2010like cellular injury. Cell viability was determined using a cell counting kit\u20108 (CCK\u20108) assay, while cell proliferation was analyzed through a 5\u2010Ethynyl\u20102\u2032\u2010deoxyuridine assay. Cell apoptosis was measured using flow cytometry, and enzyme\u2010linked immunosorbent assays were performed to detect levels of pro\u2010inflammatory cytokines IL\u20106 and TNF\u2010\u03b1. Additionally, Fe<jats:sup>2+<\/jats:sup> levels were analyzed using a colorimetric assay kit, reactive oxygen species (ROS) levels were assessed with a Cellular ROS Assay kit, and lipid peroxidation was measured using a malondialdehyde assay kit. Glutathione levels were analyzed with a detection assay. Protein and mRNA expression were evaluated through western blotting and quantitative real\u2010time polymerase chain reaction, respectively. Furthermore, an RNA immunoprecipitation assay was conducted to investigate the association between ELAV\u2010like RNA binding protein 1 (ELAVL1) and SOAT2. Actinomycin D assay was performed to explore the effect of ELAVL1 depletion on the transcript stability of SOAT2 mRNA. SOAT2 and ELAVL1 expression were upregulated in caerulein\u2010exposed AR42J cells. Caerulein treatment induced pancreatitis\u2010like cellular apoptosis, inflammatory response, ferroptosis, and cell proliferation inhibition. Silencing of SOAT2 protected against caerulein\u2010induced AR42J cell injury. Moreover, ELAVL1 stabilized SOAT2 mRNA expression in AR42J cells. SOAT2 overexpression attenuated the effects induced by ELAVL1 silencing in caerulein\u2010exposed AR42J cells. Additionally, ELAVL1 knockdown activated the NRF2\/HO\u20101 pathway by downregulating SOAT2 expression in caerulein\u2010exposed AR42J cells. SOAT2 silencing protected AR42J cells from caerulein\u2010induced injury by inactivating the NRF2 pathway. In conclusion, ELAVL1\u2010dependent SOAT2 exacerbated pancreatic exocrine cell injury by inactivating the NRF2\/HO\u20101 pathway in pancreatitis. These findings provide new insights into the molecular mechanisms underlying pancreatitis and offer potential therapeutic targets for the treatment of this condition.<\/jats:p>","DOI":"10.1002\/kjm2.12911","type":"journal-article","created":{"date-parts":[[2024,11,26]],"date-time":"2024-11-26T11:55:19Z","timestamp":1732622119000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["<scp>ELAVL1<\/scp>\u2010dependent <scp>SOAT2<\/scp> exacerbated the pancreatitis\u2010like cellular injury of <scp>AR42J<\/scp> cells induced by hyperstimulation with caerulein"],"prefix":"10.1002","volume":"41","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-8265-0766","authenticated-orcid":false,"given":"Yu\u2010Jing","family":"Sun","sequence":"first","affiliation":[{"name":"Emergency Department Zhongshan Hospital of Xiamen University  Xiamen Fujian 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