Acute pancreatitis (AP) is an inflammatory disease caused by the abnormal activation of pancreatic enzymes in the pancreas, with a considerably high morbidity and mortality. However, the etiological factor and pathogenesis of AP are still unclear. This study was aimed to explore the role and mechanism of interferon regulatory factor 9 (IRF9) in the occurrence of AP and to provide experimental and theoretical foundation for AP diagnosis and treatment. AP model in vitro was established by caerulein-induced group. Small interfering RNA (siRNA) was designed and constructed to silence IRF9 gene. After siRNA transfected and caerulein treated successfully, the expression levels of IRF9, SIRT1, and acetylated p53 (Ac-p53) were determined by qRT-PCR and Western blot. The apoptosis, proliferation, and migration of AR42J cells were checked by flow cytometry, MTT, and transwell assay. Dual-luciferase reporter assay was implemented to validate the regulatory effect of IRF9 on SIRT1. Here, our study showed that the expression of IRF9 and Ac-p53 was increased, SIRT1 was decreased, and cell apoptosis, proliferation, and migration of AR42J cells were increased after caerulein induced. IRF9 gene silencing upregulated SIRT1, downregulated Ac-p53, and inhibited cell apoptosis, proliferation, and migration. Dual-Luciferase reporter assay showed that IRF9 could negatively regulate SIRT1. The potential mechanism was that IRF9 could modulate cell apoptosis, proliferation, migration, and bind the promoter of SIRT1 to repress SIRT1-p53. It hinted that IRF9 showed a novel function in AP by modulating cell apoptosis, proliferation, migration, and suppressing SIRT1-p53. IRF9 might be a good potential treatment target for AP.

急性胰腺炎（AP）是由胰腺中胰腺酶的异常激活引起的炎性疾病，其发病率和死亡率相当高。然而，AP的病因和发病机制仍不清楚。本研究旨在探讨干扰素调节因子9（IRF9）在AP发生中的作用和机制，为AP的诊断和治疗提供实验和理论基础。由caerulein诱导组建立体外AP模型。设计并构建了小干扰RNA（siRNA）以沉默IRF9基因。成功转染siRNA并用caerulein处理后，通过qRT-PCR和Western blot检测IRF9，SIRT1和乙酰化p53（Ac-p53）的表达水平。流式细胞仪检测AR42J细胞的凋亡，增殖和迁移，MTT和transwell分析。实施双重荧光素酶报告基因测定以验证IRF9对SIRT1的调节作用。在这里，我们的研究表明，在由青霉素诱导后，IRF9和Ac-p53的表达增加，SIRT1减少，AR42J细胞的细胞凋亡，增殖和迁移增加。IRF9基因沉默上调SIRT1，下调Ac-p53，并抑制细胞凋亡，增殖和迁移。双重荧光素酶报告基因测定表明IRF9可以负调控SIRT1。潜在的机制是IRF9可以调节细胞凋亡，增殖，迁移并结合SIRT1的启动子来抑制SIRT1-p53。这暗示IRF9通过调节细胞凋亡，增殖，迁移和抑制SIRT1-p53而在AP中显示出新功能。