组织细胞间粘附分子-1在阻塞性黄疸小肠粘膜损伤中的作用及丹参防治机制的研究

目的：研究组织细胞间粘附分子－1（ICAM－1）在阻塞性黄疸（阻黄）小肠粘膜损伤中的作用及丹参防治小肠粘膜损伤机制。方法：SD大鼠48只分为4组：假手术对照组（SO＋NS）、阻黄组（BDL＋NS）、治疗对照组（SO＋SM）及丹参治疗组（BDL＋SM），每组术后再随机分设7、14d两个时相点。在不同时相点检测小肠组织髓过氧化物酶活性（MPO）、ICAM－1、二胺氧化酶（DAO）、血浆内毒素水平变化，并与丹参治疗组进行比较。结果：BDL＋NS组7、14d时小肠DAO的活性降低，MPO活性增高P＜0．05），门表脉血浆内毒素增加，ICAM－1主要表达在小肠粘膜上皮组织，且表达逐渐增强（P＜0．05）；BDL＋SM组7、14d时小肠组织DAO活性显著升高，门静脉血浆内毒素降低，ICAM－1表达受到抑制（P＜0．05），MPO改变不明显。结论：阻黄引起小肠上皮细胞上的ICAM－1表达上调，参与了中性粒细胞（PMN）介导的小肠粘膜损伤；丹参是通过抑制ICAM－1的表达而减轻小肠粘膜的损伤。

Effect of intercellular adhesion molecule-1 on enteromucosal injury in rats with obstructive jaundice

Objective To study the effect of intercellular adhesion molecule-1 (ICAM-1) on en-teromucosal injury in rats with obstructive jaundice and the preventive and therapeutic mechanism of salviae miltiorrhizae (SM).Methods Fourty-eight SD rats were randomly divided into 4 groups:sham operation (SO+ NS), bile duct-ligation (BDL + NS), sham operation + SM (SO+ SM), bile duct-ligation + SM (BDL+ SM). Each group was randomly divided into subgroups of day 7 and 14. ICAM-1 protein was detected by immunohistochemistry staining. Intestinal activity of myeloperioxidase (MPO), intestinal activity of diamine oxidase (DAO), portal vein blood endotoxin were examined on the 7th and 14th day. The results were compared with those obtained from SM groups. Results On the 7th and 14th day after bile duct-ligation, intestinal DAO activity was decreased, intestinal MPO activity and portal vein blood endotoxin increased( P <0.05), the ICAM-1 protein was mainly expressed on intestinal epithelia and in-creased( P <0.05)in BDL+ NS group. In the BDL+ SM group, intestinal DAO activity was increased, portal vein blood endotoxin decreased and the ICAM-1 expression was inhibited by SM on the 7th and 14th day after bile duct-ligation( P <0. 05), but SM had no influence on the intestinal MPO activity. Conclusion The ICAM-1 expression was up-regulated after bile duct-ligation and might be involved in PMN-mediated injury to intestinal mucosa;SM might displayed its preventive and therapeutic effects by way of ICAM-1 expression down-regulation.