摘要
目的研究异氟烷对大鼠肝脏缺血再灌注损伤后细胞间黏附分子-1(ICAM-1)的影响,探讨异氟烷肝脏缺血再灌注保护作用的机制。方法将32只SD成年雌性大鼠分为假手术组、缺血再灌注组、异氟烷组、异氟烷-缺血再灌注组。假手术组、异氟烷组作为对照;缺血再灌注组和异氟烷-缺血再灌注组阻断支配大鼠肝脏左叶和中叶的门静脉分支,建立肝脏70%缺血再灌注模型,缺血60min再灌注3h后取材,测定大鼠血清ALT、AST;免疫组织化学方法检测ICAM-1蛋白的表达,HE染色进行病理学检查。结果肝脏缺血60min再灌注3h后肝组织ICAM-1蛋白表达水平增高;血清酶ALT和AST升高;肝组织损害严重。异氟烷抑制ICAM-1表达,降低ALT、AST水平,减轻肝细胞损伤。结论肝脏缺血再灌注损伤程度与肝组织内ICAM-1水平有密切的关系,异氟烷可抑制肝脏缺血再灌注期间肝组织ICAM-1的表达,同时减轻伤肝脏损伤。
Objective To investigate the role of intercellular adhesion molecule-1 （ICAM-1） in Isoflurane against hepatic ischemia-reperfusion （I/R） injury in vivo. Methods Thirty-two female SD rats were randomly min after hepatic ischemia. The animals were killed 3 h after reperfusion, then and blood were obtained. ALT and AST in blood serum were detected as liver damage specimens of liver tissues markers. The histological examination of liver tissues was done by hematoxylin and eosin staining. The levels of ICAM-1 protein in the hedamage Isoflurane significantly inhibited the ICAM-1 expression. Conclusion The degree of hepatic ischemi- a-reperfusion injury is closely associated with the expression level of ICAM-1. Isoflurane abates liver ischemiareperfusion injury and inhibits the ICAM-1 expression.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2008年第3期241-243,共3页
Journal of Third Military Medical University
关键词
异氟烷
缺血再灌注损伤
细胞间黏附分子-1
Isoflurane
ischemia-reperfusion injury
intercellular adhesion molecule-1
