Acute pancreatitis (AP) is a dysfunctional pancreas disease marked by severe inflammation. Long non-coding RNAs (lncRNAs) involving in the regulation of inflammatory responses have been frequently mentioned. The purpose of this study was to ensure the function and action mode of lncRNA maternally expressed gene 3 (MEG3) in caerulein-induced AP cell model. HPDE cells were treated with caerulein to establish an AP model in vitro. The expression of MEG3, miR-195-5p, and fibroblast growth factor receptor 2 (FGFR2) was measured using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation and apoptosis were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry assay, respectively. The expression of CyclinD1, B cell lymphoma/leukemia-2 (Bcl-2), Bcl-2-associated X protein (Bax), FGFR2, P65, phosphorylated P65 (p-P65), alpha inhibitor of nuclear factor kappa beta (NF-κB) (IκB-α), and phosphorylated IκB-α (p-IκB-α) at the protein level was quantified by western blot. The concentrations of tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) were monitored by enzyme-linked immunosorbent assay (ELISA). The targeted relationship between miR-195-5p and MEG3 or FGFR2 was forecasted by the online software starBase v2.0 and verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. As a result, the expression of MEG3 and FGFR2 was decreased in caerulein-induced HPDE cells, while the expression of miR-195-5p was increased. MEG3 overexpression inhibited cell apoptosis and inflammatory responses that were induced by caerulein. Mechanically, miR-195-5p was targeted by MEG3 and abolished the effects of MEG3 overexpression. FGFR2 was a target of miR-195-5p, and MEG3 regulated the expression of FGFR2 by sponging miR-195-5p. FGFR2 overexpression abolished miR-195-5p enrichment-aggravated inflammatory injuries. Moreover, the NF-κB signaling pathway was involved in the MEG3/miR-195-5p/FGFR2 axis. Collectively, MEG3 participates in caerulein-induced inflammatory injuries by targeting the miR-195-5p/FGFR2 regulatory axis via mediating the NF-κB pathway in HPDE cells.

急性胰腺炎 (AP) 是一种以严重炎症为特征的功能失调的胰腺疾病。涉及炎症反应调节的长链非编码 RNA (lncRNA) 经常被提及。本研究的目的是确保lncRNA母源表达基因3（MEG3）在雨蛙肽诱导的AP细胞模型中的功能和作用模式。HPDE细胞用雨蛙素处理体外建立AP模型. 使用定量实时聚合酶链反应 (qRT-PCR) 测量 MEG3、miR-195-5p 和成纤维细胞生长因子受体 2 (FGFR2) 的表达。细胞增殖和凋亡分别通过3-(4, 5-二甲基-2-噻唑基)-2,5-二苯基-2-H-溴化四唑(MTT)法和流式细胞术检测。CyclinD1、B细胞淋巴瘤/白血病-2（Bcl-2）、Bcl-2相关X蛋白（Bax）、FGFR2、P65、磷酸化P65（p-P65）、核因子κβ（NF）的α抑制剂的表达-κB) (IκB-α) 和蛋白质水平的磷酸化 IκB-α (p-IκB-α) 通过蛋白质印迹定量。通过酶联免疫吸附试验 (ELISA) 监测肿瘤坏死因子 α (TNF-α)、白介素-1β (IL-1β) 和白介素-6 (IL-6) 的浓度。miR-195-5p 与 MEG3 或 FGFR2 之间的靶向关系由在线软件 starBase v2.0 预测，并通过双荧光素酶报告基因检测和 RNA 免疫沉淀 (RIP) 检测验证。结果，在雨蛙素诱导的HPDE细胞中MEG3和FGFR2的表达降低，而miR-195-5p的表达增加。MEG3 过表达抑制了由雨蛙素诱导的细胞凋亡和炎症反应。机械上，miR-195-5p 被 MEG3 靶向并消除了 MEG3 过表达的影响。FGFR2 是 miR-195-5p 的靶点，MEG3 通过吸附 miR-195-5p 来调节 FGFR2 的表达。FGFR2 过表达消除了 miR-195-5p 富集加重的炎症损伤。此外，NF-κB 信号通路参与 MEG3/miR-195-5p/FGFR2 轴。总的来说，