摘要
目的:探讨大鼠全脑缺血再灌注时脑组织血红氧化酶-1(HO-1)活性及全血炭氧血红蛋白(COHb)含量的变化在脑损伤中的作用。方法:42只SD大鼠分为假手术组(S组)7只,脑缺血再灌注组(I组)35只。将I组大鼠制作为全脑缺血再灌注模型,模型成功后1 h,处死S组大鼠;I组分别于1、3、12、24及48 h时各处死7只,分别检测各组大鼠脑组织HO-1活性及一氧化碳(CO)和cGMP含量;计数海马CA1区单位面积神经元存活数。结果:①模型建立1 h时脑组织HO-1、COHb及cGMP含量即达高峰,后逐渐降低,于3 h后又逐渐升高,至48 h再次达第2次高峰。②与S组比较,I组海马CA1区神经元存活数在模型建立1 h时无明显变化,3 h后显著减少,至48 h仍维持于1较低水平。结论:脑缺血再灌注时脑内HO-1高度表达,内源性CO水平升高,提示HO-CO-cGMP系统可能在脑缺血再灌注损伤中起重要作用。
Objective： To observe the change of hemeoxygenase-1 （HO-1） activity in cerebral tissue, carboxyhemo- globin （COHb） in blood of rats during global cerebral ischemia-reperfusion. Methods： Cerebral ischemia-reperfusion model was produced in SD rats. In sham （S） group and ischemia-reperfusion （I） group HO-1 activity, cyclic GMP （cGMP） in the brain and COHb in blood were evaluated respectively at 1, 3, 12, 24 and 48 h during global cerebral ischemia and reperfusion, and the surviving number of pyramidal cells in hippocampus CA1 was assessed. Results： （1） HO-1 activity, COHb content and cGMP levels in I group peaked at 1 h during global cerebral ischemia and reperfusion, then decreased gradually, and at 3 h began to increase, peaked more at 48 h. （2） As compared with S group,,the surviving number of pyramidal cells in hippocampus CA1 of I group did not change significantly at 1 h, then decreased markedly, lasted till 48 h. Conclusion： HO-1 was highly expressed in brain of rats during global cerebral ischemia-reperfusion, and endogenous carbon monoxide increased and HO-CO-cGMP system may play an important role in the pathogenesis of global cerebral ischemia-reperfusion.
出处
《中国康复》
2008年第4期223-225,共3页
Chinese Journal of Rehabilitation
基金
湖北省卫生厅第五个三年科研计划项目资助(编号:WJ01518)
