Emodin is an effective component in rhubarb to cure intestinal dysfunction, but the specific mechanism remains unknown. This study aimed to evaluate the protective effects of emodin on intestinal dysfunction caused by acute severe pancreatitis and reveal the functional mechanism of emodin in the treatment of this condition. An acute severe pancreatitis model was prepared using taurocholate. In the treatment group, 50 mg/kg emodin was injected intravenously 2 h before the induction of acute severe pancreatitis at an interval of 8 h. After 24 h, the gene expression and protein levels of miR-218a-5p, RhoA, ROCK1, Akt, Notch1, Bax, Bcl-2, Fas, FasL, caspase-3, and caspase-9 were determined through reverse transcription polymerase chain reaction and Western blot analysis. The protein levels of occludin, zonula occludens-1 (ZO-1), and E-cadherin in the intestinal tract were also determined through Western blot analysis. The effects of miR-218a-5p on the apoptosis of rat intestinal epithelial cell-18 were observed through flow cytometry. The effects of emodin on intestinal cell apoptosis induced by acute severe pancreatitis were observed via TUNEL (terminal deoxynucleotidyl transferase dUTP nick-end labeling). Pathological changes in the pancreas and intestine of rats in each group were observed through hematoxylin and eosin staining. After 24 h of acute severe pancreatitis induced by taurocholate, emodin reduced the expression of miR-218a-5p in the intestinal tract; increased the expression of Notch1 and Bcl-2; decreased the expression levels of RhoA, ROCK1, Akt, Bax, Fas, FasL, caspase-3, and caspase-9; inhibited the intestinal cell apoptosis caused by acute severe pancreatitis; increased the protein expression levels of occludin, zonula occludens-1 (ZO-1), and E-cadherin in the intestinal tract; and alleviated intestinal dysfunction caused by acute severe pancreatitis. Emodin could regulate Notch1 and RhoA/ROCK pathways by regulating the miR-218a-5p expression in the intestine. It could also inhibit intestinal cell apoptosis induced by acute severe pancreatitis and improve the intestinal dysfunction caused by severe acute pancreatitis.

大黄素是大黄中治疗肠道功能障碍的有效成分，但具体机制尚不清楚。这项研究旨在评估大黄素对急性重症胰腺炎引起的肠道功能障碍的保护作用，并揭示大黄素在治疗该病中的功能机制。使用牛磺胆酸盐制备了急性重症胰腺炎模型。在治疗组中，在诱发急性重症胰腺炎之前2小时以8小时的间隔静脉注射50 mg / kg大黄素。24小时后，通过逆转录聚合酶链测定miR-218a-5p，RhoA，ROCK1，Akt，Notch1，Bax，Bcl-2，Fas，FasL，caspase-3和caspase-9的基因表达和蛋白质水平。反应和蛋白质印迹分析。闭合小带，闭合小带蛋白1（ZO-1），还通过蛋白质印迹分析确定了肠道中的E-钙粘蛋白和E-钙粘蛋白。通过流式细胞术观察miR-218a-5p对大鼠肠上皮细胞18凋亡的影响。通过TUNEL（末端脱氧核苷酸转移酶dUTP缺口末端标记）观察到大黄素对急性重症胰腺炎诱导的肠道细胞凋亡的影响。通过苏木精和曙红染色观察每组大鼠胰腺和肠道的病理变化。牛磺胆酸盐诱导的急性重症胰腺炎24小时后，大黄素降低肠道miR-218a-5p的表达；增加Notch1和Bcl-2的表达；降低RhoA，ROCK1，Akt，Bax，Fas，FasL，caspase-3和caspase-9的表达水平；抑制急性重症胰腺炎引起的肠道细胞凋亡；增加小肠闭合蛋白，闭合小带-1（ZO-1）和E-钙粘蛋白的蛋白表达水平；并减轻了急性重症胰腺炎引起的肠道功能障碍。大黄素可以通过调节肠中miR-218a-5p的表达来调节Notch1和RhoA / ROCK通路。它也可以抑制急性重症胰腺炎引起的肠道细胞凋亡，并改善重症急性胰腺炎引起的肠道功能障碍。