Background: The pathogenesis of Severe Acute Pancreatitis (SAP) is mediated substantially by dysfunctions in the intestinal barrier. Euphorbia kansui (EK) is a medicinal plant used widely in traditional Chinese medicine to treat inflammation; however, its efficacy and mechanism of action in SAP treatment are not yet well understood.

Objective: To investigate the role of EK in intestinal barrier tissue repair and in the pathogenesis and development of SAP.

Methods: The rat SAP model was established by a retrograde injection of sodium taurocholate into the pancreatic bile duct. The SAP model group and the SAP + EK treatment groups were divided into 6 subgroups according to timing: 2, 6, 12, 24, 48, or 72h after inducing SAP. The progression of the SAP rats and of the rats receiving the EK treatment was evaluated using the ascites volume, serum amylase and plasma endotoxin levels, and histological grading of intestinal mucosal damage. In addition, serum inflammatory factor contents were measured using Enzyme-Linked Immunosorbent Assay (ELISA) tests and apoptotic cells in damaged ileum tissue were detected using TUNEL staining. Apoptosis markers and other signaling proteins in intestinal mucosal cells were detected by immunohistochemical assays and then validated by combining these data with quantitative polymerase chain reactions and western blotting.

Results: Compared with the results of the SAP model rats, the results of the rats that received EK treatment demonstrated that EK could effectively reduce the ascites volume and serum amylase and plasma endotoxin levels. EK treatment also greatly reduced the abnormal intestinal morphological alterations in the rat SAP model and significantly downregulated the serum contents of Interleukin (IL)-1β, IL-6, and tumor necrosis factor-α. EK treatment inhibited the elevation of capapse-3, inhibited the decrease of the Bcl-2 protein, and decreased the number of apoptotic cells in rat ileum tissue. Finally, EK treatment abrogated the increase of HMGB1 and the suppression of MFG-E8 protein expression in the SAP + EK rat ileum tissue.

Conclusion: EK suppresses SAP pathogenesis by restoring the intestinal barrier function and modulating the HMGB1/MFG-E8 signaling axis.

背景：严重急性胰腺炎 (SAP) 的发病机制主要由肠道屏障功能障碍介导。甘水大戟（EK）是一种广泛用于中药治疗炎症的药用植物；然而，其在 SAP 治疗中的功效和作用机制尚不清楚。

目的：探讨EK在肠屏障组织修复及SAP发病机制中的作用。

方法：通过胰胆管逆行注射牛磺胆酸钠建立大鼠SAP模型。SAP模型组和SAP+EK治疗组按时间分为6个亚组：诱导SAP后2、6、12、24、48或72h。使用腹水量、血清淀粉酶和血浆内毒素水平以及肠粘膜损伤的组织学分级来评估 SAP 大鼠和接受 EK 治疗的大鼠的进展。此外，使用酶联免疫吸附试验 (ELISA) 测试测量血清炎症因子含量，并使用 TUNEL 染色检测受损回肠组织中的凋亡细胞。

结果：与SAP模型大鼠的结果相比，接受EK治疗的大鼠的结果表明，EK可以有效降低腹水量和血清淀粉酶和血浆内毒素水平。EK 治疗还大大减少了大鼠 SAP 模型的异常肠道形态改变，并显着下调了血清白细胞介素 (IL)-1β、IL-6 和肿瘤坏死因子-α 的含量。EK处理抑制了capapse-3的升高，抑制了Bcl-2蛋白的降低，并减少了大鼠回肠组织中凋亡细胞的数量。最后，EK 治疗消除了 SAP + EK 大鼠回肠组织中 HMGB1 的增加和 MFG-E8 蛋白表达的抑制。

结论：EK 通过恢复肠道屏障功能和调节 HMGB1/MFG-E8 信号轴来抑制 SAP 发病机制。