Background. Acute pancreatitis (AP) is a clinically frequent acute abdominal condition, which refers to an inflammatory response syndrome of edema, bleeding, and even necrosis caused by abnormal activation of the pancreas’s own digestive enzymes. Intestinal damage can occur early in the course of AP and is manifested by impaired intestinal mucosal barrier function, and inflammatory reactions of the intestinal mucosa, among other factors. It can cause translocation of intestinal bacteria and endotoxins, further aggravating the condition of AP. Therefore, actively protecting the intestinal mucosal barrier, controlling the progression of intestinal inflammation, and improving intestinal dynamics in the early stages of AP play an important role in enhancing the prognosis of AP. Methods. The viability and apoptosis of RAW264.7 cells treated with Esculentoside A (EsA) and/or lipopolysaccharide were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry, respectively. The expression of apoptosis-related proteins and NF-κB signaling pathway-related proteins were detected by western blot (WB). An enzyme-linked immunosorbent assay was used to measure TNF-α and IL-6 secretion. Results. In vitro experiments demonstrated that EsA not only promoted the apoptosis of inflammatory cells but also reduced the secretion of TNF-α and IL-6 in a dose-dependent manner. Additionally, it inhibited the activation of the NF-κB signaling pathway by decreasing the expression of phosphorylated-p65(p-p65) and elevating the expression of IκBα. Similarly, in vivo experiments using a rat AP model showed that EsA inhibited the expression of p-p65 elevating the expression of IκBα in the intestinal tissues of the rat AP model and promoting the apoptosis of inflammatory cells in the intestinal mucosa in vivo experiments, while improving the pathological outcome of the pancreatic and intestinal tissues. Conclusion. Our results suggest that EsA can reduce intestinal inflammation in the rat AP model and that EsA may be a candidate for treating intestinal inflammation in AP and further arresting AP progression.

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EsA 通过 NF-κB 通路改善急性胰腺炎肠道炎症的相关研究

背景。急性胰腺炎（AP）是临床上常见的急腹症，是指胰腺自身消化酶异常激活引起的水肿、出血甚至坏死的炎症反应综合征。肠道损伤可发生在AP病程早期，表现为肠粘膜屏障功能受损、肠粘膜炎症反应等。它会引起肠道细菌和内毒素的移位，进一步加重AP的病情。因此，在AP早期积极保护肠黏膜屏障、控制肠道炎症进展、改善肠道动力学对于改善AP预后具有重要作用。方法。使用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四唑(MTT)和流式细胞术检测用Esculentoside A (EsA)和/或脂多糖处理的RAW264.7细胞的活力和凋亡。分别。采用蛋白质印迹（WB）检测凋亡相关蛋白和NF-κB信号通路相关蛋白的表达。使用酶联免疫吸附测定法测量 TNF- α和 IL-6 的分泌。结果。体外实验表明，EsA不仅促进炎症细胞凋亡，而且呈剂量依赖性减少TNF- α和IL-6的分泌。此外，它还通过降低磷酸化-p65(p-p65)的表达和升高IκBα的表达来抑制NF - κB信号通路的激活。同样，大鼠AP模型的体内实验表明，EsA抑制p-p65的表达，升高大鼠AP模型肠组织中IκBα的表达，促进体内肠粘膜炎症细胞的凋亡实验，同时改善胰腺和肠道组织的病理结果。结论。我们的结果表明，EsA 可以减轻大鼠 AP 模型中的肠道炎症，并且 EsA 可能是治疗 AP 肠道炎症并进一步阻止 AP 进展的候选药物。