肢体缺血-再灌注后大鼠心肌中的氧化应激及HO-1mRNA表达  

Oxidative stress and expression of heme oxygenase-1 mRNA in the myocardial tissue of rats after limb ischemia/reperfusion injury

作　　者：李艳艳[1] 袁锋[2] 陈丹[2] 朱付平[2] 熊光仲[2] 

机构地区：[1]上海市徐汇区中心医院急诊科,上海200031 [2]中南大学湘雅二医院急诊科

出　　处：《中华急诊医学杂志》2010年第5期516-521,共6页Chinese Journal of Emergency Medicine

摘　　要：目的探讨肢体缺血．再灌注损伤后心肌的氧化损伤机制及HO-1的保护作用，为研究肢体缺血-再灌注损伤所致的心肌损伤的预防提供实验依据。方法应用止血带构造SD大鼠双后肢IR模型，实验动物随机（随机数字法）分为正常对照组和缺血4h再灌注2h，4h，6h，8h，16h，24h共7组，分别取心肌和血液标本检测MDA，SOD，MPO，心肌形态学及心肌组织中HO-1mRNA的表达。方差分析方法进行统计学处理。结果（1）血浆及心肌IR各组MDA均较对照组明显升高（P〈0．05），且于IR4h达高峰。血浆及心肌IR各组SOD均较对照组明显降低（P〈0．05），且血清SOD于IR4h达最低值，心肌SOD于IR8h达最低值。血浆及心肌IR各组MPO均较对照组明显升高（P〈0．05），且血清MPO于IR4h达高峰，心肌MPO于IR6h达高峰。（2）在肢体缺血4h再灌注4～6h组，心肌形态学损伤最重。（3）与对照组比较，IR2h组HO-1mRNA表达差异无统计学意义（P〉0．05），其余各组HO-1mRNA表达均显著上调（P〈0．05）且于IR16h达高峰。结论心肌局部组织的自由基和中性粒细胞聚集活化是LIR心肌损伤的机制且能上调HO-1mRNA的表达，HO-1在心肌组织的高表达能减轻心肌组织的损伤。Objective To study the mechanism of oxidative damage in myocardial tissue after limb ischemia reperfusion （IR）, and the protective effects of heine oxygenase-1 on myocardial injury in experimental rats. Method The models of bilateral hind limbs ischemia and reperfusion in rats were established by using tourniquets applied to the roots of both hind limbs until palm blanched and pulseless for 4 hours. A total of 56 SD rats were randomly （random number） divided into 7 groups, namely one normal control group （ n = 8） and 6 ischemia- reperfusion groups as per different lengths of repeffusion time, e.g. 2 hrs, 4 hrs, 8 hrs, 16 h rs and 24 hr （ n = 8 each）. The experimental rats were sacrificed after different lengths of reperfusion time. Specimens of myocardium and blood were taken for assays of malonaldehyde （MDA）, superoxide dismutase （SOD） and myeloperoxidase （MPO）, and pathological changes of myocardium were observed, and the expressions of HO-1 mRNA in myocardium were detected. Data were analyzed with ANOVA. Results （1） Compared with the control group, the levels of serum MDA and myocardial MDA of rats were increased in all IR groups and were higher （ P 〈 0.05 ）, and the levels of MDA reached the peak after repeffusion for 4 hours. The levels of serum SOD and myocardial SOD in rats of all IR groups were decreased and lower than those in rats of the control group （ P 〈 0.05）, and the levels of serum SOD dropped away to the lowest point after reperfusion for 4 hours, and the levels of myocardial SOD fell off to the bottom after reperfusion for 8 hours. The levels of serum MPO and myocardial MPO were significantly increased in rats of all IR groups compared with the control group （ P 〈 0.05）. The levels of serum MPO reached peak after reperfusion for 4 hours, and the levels of myocardial MPO were increased to the highest spot after reperfusion for 6 horns. （2） The pathological changes in myocardium showed the most severe damage after reperfusion for 4 - 6 hours. �

关 键 词：缺血-再灌注 血红素加氧酶-1 氧化应激 心肌 肢体 丙二醛 髓过氧化物酶 超氧化物歧化酶 

分 类 号：R285.5[医药卫生—中药学]