Anhui University of Science and Technology, Huainan, 232001, China.
Department of Gastroenterology, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai, China.
Pancreatology. 2022 Jan;22(1):74-82. doi: 10.1016/j.pan.2021.11.004. Epub 2021 Nov 9.
Post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP) is the most common complication following ERCP and the mechanism is not fully understood. This study evaluated the changes in the inflammatory response, cellular apoptosis, and tight junction integrity in a rat model of pancreatitis to explore the underlying mechanism.
PEP was induced in rats by retrograde biliopancreatic ductal infusion of contrast agents or saline. Pancreatic tissues were harvested and evaluated by histopathologic, immunohistochemical, immunofluorescence, and Western blot analyses. In addition, amylase and proinflammatory cytokines in plasma were quantified by ELISA assay.
PEP rats developed more severe acute pancreatitis than the sham group after injection of the contrast agent or isotonic saline. PEP rats exhibited increased tissue damage, plasma amylase, proinflammatory cytokines, necrosis, inflammatory infiltrates, apoptosis, and tight junction disruption. At the molecular level, contrast agent and isotonic saline-injected PEP rats demonstrated elevated NF-κB p65 and STAT3 pathways activation, altered expression and activation of apoptosis-related proteins, and suppressed expression of tight junction molecules. However, the contrast agent concentration had no effect on these changes.
In models of acute pancreatitis induced using contrast agent and hydrostatic pressure, the contrast agent and high hydrostatic pressure easily induced the inflammatory response, apoptosis, and tight junction disruption. It is noteworthy that no significant difference in damaged pancreatic acinar cells was observed with different concentrations of the contrast agent.
内镜逆行胰胆管造影（ERCP）后胰腺炎（PEP）是 ERCP 后最常见的并发症，其机制尚不完全清楚。本研究通过建立大鼠模型评估胰腺炎中炎症反应、细胞凋亡和紧密连接完整性的变化，以探讨其潜在机制。
通过逆行胰胆管内注射造影剂或生理盐水诱导 PEP 大鼠模型。通过组织病理学、免疫组织化学、免疫荧光和 Western blot 分析采集和评估胰腺组织。此外，通过 ELISA 测定血浆中淀粉酶和促炎细胞因子的含量。
与假手术组相比，注射造影剂或等渗盐水后的 PEP 大鼠发生更严重的急性胰腺炎。PEP 大鼠表现出组织损伤加重、血浆淀粉酶、促炎细胞因子、坏死、炎症浸润、凋亡和紧密连接破坏增加。在分子水平上，造影剂和等渗盐水注射的 PEP 大鼠中 NF-κB p65 和 STAT3 途径被激活，凋亡相关蛋白的表达和激活发生改变，紧密连接分子的表达受到抑制。然而，造影剂浓度对这些变化没有影响。
在使用造影剂和静水压力诱导的急性胰腺炎模型中，造影剂和高静水压力容易引起炎症反应、细胞凋亡和紧密连接破坏。值得注意的是，不同浓度的造影剂对受损胰腺腺泡细胞没有明显差异。
