大黄素对重症急性胰腺炎致全身炎症反应综合征大鼠腹腔巨噬细胞ICAM-3的体外作用

摘要

目的 研究在重症急性胰腺炎(SAP)导致全身炎症反应综合征(SIRS)的大鼠模型中,大黄素和地塞米松体外对腹腔巨噬细胞细胞间黏附因子(ICAM)-3蛋白表达水平的变化.方法 经胆胰管逆行注入1.5％去氧胆酸钠溶液制备大鼠SAP/SIRS模型.重症急性胰腺炎SIRS模型制备:20只SD大鼠随机分为假手术组和重症急性胰腺炎SIRS模型组,每组10只.体外干预实验:将假手术组取出的腹腔巨噬细胞单独设为1组；将重症急性胰腺炎SIRS模型组取出的腹腔巨噬细胞分为大黄素干预组、地塞米松干预组、对照组.结果 ①胰腺组织病理学改变:与假手术组比较,SIRS模型组具有显著性病理改变.②各组大鼠腹腔巨噬细胞吞噬凋亡PMN能力比较差异均有统计学意义(P＜0.05).③流式细胞仪检测各组细胞ICAM-3表达情况比较差异均有统计学意义(P＜0.05).④免疫荧光技术检测各组细胞ICAM-3表达情况比较差异均有统计学意义(P＜0.05).结论 大黄素可能通过改变巨噬细胞的胞膜ICAM-3的表达水平,增强腹腔巨噬细胞吞噬及清除凋亡细胞的能力.%Objective To determine the variation in intracellular adhesion molecule-3 (ICAM-3) expression in extracorporeal peritoneal macrophage (pMΦ) as a result of emodin and dexamethasone administration in rats with severe acute pancreatitis (SAP) followed by systemic inflammatory response syndrome (SIRS). Methods The SAP/SIRS rat models were constructed via retrograde injection of 1.5% sodium deoxycholate into the common biliopancreatic duct. A total of 20 rats with SAP/SIRS were randomly divided into Sham operation group (n=10) and SAP/SIRS model group (n=10), respectively. This was followed by further allocation into group so using pMΦs in Sham operation group as well as emodin treatment group (group EMO), dexamethasone treatment group (group DEX) and control group (group CON) using pMΦs in SAP/SIRS group. Results SAP/SIRS model group yielded considerable pathologic variation in the pancreatic tissues as compared with Sham operation group. The capacity of pMΦs for apoptotic PMN clearance was lowered in SAP/SIRS rat models compared with sham-operated rats, but significantly elevated in the group EMO or group DEX compared with controls, and in the group EMO compared with group DEX. The level of I-CAM-3 expression as measured by flow cytometry was remarkably lowered in SAP/SIRS model rats as compared with the sham-operated group, significantly elevated in the group EMO or group DEX as compared with the control group, and also higher in the group EMO as compared with the group DEX. The level of ICAM-3 expression as measured by immunofluorescence assay was remarkably lowered in SAP/SIRS model rats as compared with the sham-operated group but significantly elevated in the group EMO or group DEX as compared with the control group. Conclusion Emodin may promote phagocytosis of PMΦ and elimination of apoptotic cells via altering ICAM-3 expression on the membrane of macrophages.