青藤碱抗大鼠肝脏缺血/再灌注损伤作用的机制探讨  

Protective mechnism of sinomenine on hepatic injury induced by ischemia/reperfusion in rats

作　　者：李淑翠[1] 李庆忠[1] 王垣芳[1] 刘金苹[1] 张树平[1] 

机构地区：[1]滨州医学院药理学教研室,山东滨州256603

出　　处：《现代生物医学进展》2010年第15期2862-2864,共3页Progress in Modern Biomedicine

基　　金：滨州医学院科技计划(BY2006KJ18)项目

摘　　要：目的:观察青藤碱对大鼠肝脏缺血再灌注损伤的影响,探讨其保护大鼠肝脏缺血再灌注损伤作用的机制。方法:通过建立大鼠全肝缺血再灌注损伤模型,应用硝酸酶还原法测定肝脏缺血再灌注后60min血清NO水平变化;测定再灌注60min后肝组织内MDA和SOD含量变化;再灌注60min取肝组织完成肝组织显微结构的观察。结果:肝脏缺血再灌注损伤后血清NO水平降低;青藤碱能提高再灌注后血清NO水平,且能改善肝脏缺血再灌注损伤的微循环,减轻肝细胞内超微结构的损害程度。结论:青藤碱对大鼠肝脏缺血再灌注损伤有保护作用,其主要作用机制是清除氧自由基和改善微循环。Objective：To investigate the protective effects of sinomenine on hepatic injury during ischemia/reperfusion proce-dure, and to investigate the posssible mechanism.Methods：40 SD rats were randomly divided into 4 groups （n=10） ：control group, I/R group, sinomenine group 1 （50mg/kg） , sinomenine group 2 （100mg/kg）.Hepatic ischemia/reperfusion models were established.At the end of reperfusion, the NO, the SOD and MDA of each group were detected.Results：In sinomenine groups the NO was higherthan that in I/R group （P0.01）.The SOD of hepatic tissue was higherin sinomenine groups than that in I/R group （P0.01）; While MDA levels were lowerin sinomenine groups than that in I/R group （P0.01）.And abnormal morphological changes of liverduring I/R procedure were remarkable in sinomenine groups.Conclusions：Sinomenine was good for the hepatic injury of ischemia/reperfusion by inhibiting the production of oxygenic free radicals and improving the function of microcirculation.

关 键 词：大鼠 青藤碱 肝脏缺血再灌注损伤 一氧化氮 

分 类 号：Q95-3[生物学—动物学] R657.3[医药卫生—外科学]