细胞间黏附分子-1抑制参与大鼠小肠缺血后处理的保护作用

ICAM-1 Inhibition Involving Small Intestinal Protection Induced by Ischemic Postconditioning in Rats

目的观察缺血后处理(I-postC)对缺血/再灌注(I/R)大鼠小肠组织细胞间黏附分子-1(ICAM-1)表达和髓过氧化物酶(MPO)活性的影响,探讨其减轻I/R损伤的机制。方法32只健康雄性Wistar大鼠随机分为假手术(Sham)、I/R、I-postC及缺血预处理(IPC)组,以无创动脉夹夹闭肠系膜上动脉建立小肠I/R损伤模型,常规制备病理切片,光镜下观察肠组织损伤情况。试剂盒测定MPO、超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量,免疫印迹法检测小肠组织ICAM-1和NF-κBP65的表达。结果I-postC明显减轻I/R导致的小肠组织病理变化,抑制I/R所致的小肠组织MPO活性和MDA含量升高(分别为I/R组的68.7%和77.1%,P<0.05),上调SOD活性(为I/R组的1.2倍,P<0.05),并下调小肠组织NF-κBP65和ICAM-1表达(分别较I/R组低44.3%和49.0%,P<0.01)。结论I-postC通过抑制ICAM-1表达和中性粒细胞游出而减轻小肠I/R损伤。

Objective To investigate the mechanisms underlying amelioration of ischemia/reperfusion （I/R） injury of ischemic postconditioning（I-postC） by studying the expression of intercellular adhesion molecule-1（ICAM-1） and myeloperoxidase（MPO） activity in small intestine subjected to Ischemia/Reperfusion, Methods 32 male Wistar rats were randomly divided into sham, I/R, I-postC and ischemic preconditioning （IPC） groups. Model of small intestinal /JR injury was made by clamping super mesenteric artery（SMA） for 45 min followed by 120 min of reperfusion in rats. HE staining was used to observe the pathology of guts of rats, Myeloperoxidase（MPO）, superoxide dismutase（SOD） activities and Malondialehyde（MDA） content in small intestine were detected. The expressions of NF-κB P65 and ICAM-1 in small intestine were detected by Western blot analysis. Results I-postC alleviated significantly the pathologic lesion of small intestine induced by/JR. The levels of MDA content and MPO activity were lower and SOD activity was higher in I-postC group than those in/JR group（ P 〈 0.05）. I/R-induced upregulation of NF-KB P65 and ICAM-1 were relieved by I- postC（ P 〈 0.01 vs. /JR group）. Conclusion I-postC protects small intestine from/JR injury through inhibiting the expression of ICAM-1 and the infiltration of PMN.