Acute pancreatitis (AP) is a common acute abdominal disease with high mortality and mortality rates. Increasing evidences clarified that Traditional Chinese Medicine (TCM) adjuvant therapy for AP can be used and it gives a positive effect. Quercetin (3,3′,4′,5,7-pentahydroxyflavone, QE) is a type of flavone compound with positive effect on cancer and inflammation prevention. The current study aims to identify the effect of QE on AP and potential molecular effect. In this case, caerulein (CAE) induced AP cell and mice model were used. QE alleviated inflammatory mediators TNF-α, IL-6, and IL-10 in experiments. In addition, miR-216b was increased based on QE treatment. In further study, MAP2K6 of p38/MAPK signaling pathway was identified as a direct target of miR-216b, and QE inhibited p38/MAPK signaling pathway through up-regulating miR-216b. Our study also first confirmed that long non-coding RNA NEAT1 is a direct target of miR-216b and can be suppressed by QE. Because of the target, NEAT1, miR-216b, and MAP2K6 formed a competitive endogenous RNA (ceRNA) network. Besides direct target mediated by QE, it also decreased TNF-α which down-regulated TRAF2 and MAP3K5 located on upstream of p38/MAPK signaling and formed a feedback loop. In conclusion, QE has a protective effect on AP through inhibiting p38/MAPK signaling pathway by up-regulating miR-216b and suppressing TNF-α.

急性胰腺炎（AP）是一种常见的急腹症，病死率和死亡率都很高。越来越多的证据表明，可以使用中医（TCM）辅助治疗 AP 并产生积极的效果。槲皮素 (3,3',4',5,7-pentahydroxyflavone, QE) 是一种对癌症和炎症预防具有积极作用的黄酮化合物。目前的研究旨在确定量化宽松对 AP 的影响和潜在的分子效应。在这种情况下，使用了卡鲁兰 (CAE) 诱导的 AP 细胞和小鼠模型。在实验中，QE 减轻了炎症介质 TNF-α、IL-6 和 IL-10。此外，基于 QE 处理，miR-216b 增加。在进一步的研究中，p38/MAPK信号通路的MAP2K6被确定为miR-216b的直接靶点，QE通过上调miR-216b抑制p38/MAPK信号通路。我们的研究还首次证实，长链非编码 RNA NEAT1 是 miR-216b 的直接靶标，可以被 QE 抑制。由于靶点，NEAT1、miR-216b和MAP2K6形成了竞争性内源RNA（ceRNA）网络。除了 QE 介导的直接靶点外，它还降低了 TNF-α，后者下调了位于 p38/MAPK 信号上游的 TRAF2 和 MAP3K5，并形成了反馈回路。综上所述，QE通过上调miR-216b和抑制TNF-α来抑制p38/MAPK信号通路对AP具有保护作用。它还降低了 TNF-α，后者下调了位于 p38/MAPK 信号上游的 TRAF2 和 MAP3K5，并形成了反馈回路。总之，QE通过上调miR-216b和抑制TNF-α来抑制p38/MAPK信号通路对AP具有保护作用。它还降低了 TNF-α，后者下调了位于 p38/MAPK 信号上游的 TRAF2 和 MAP3K5，并形成了反馈回路。总之，QE通过上调miR-216b和抑制TNF-α来抑制p38/MAPK信号通路对AP具有保护作用。