血红素氧合酶-1在大鼠实验性脑出血中的作用机制

目的探讨血红素氧合酶-1（HO-1）在大鼠实验性脑出血（ICH）脑损伤中的作用。方法采用立体定向法将自体浓缩红细胞注入大鼠基底节制作实验动物模型，通过免疫组化、干湿重法观察术后各个时间点血肿周围脑组织HO-1的表达及脑组织含水量的变化并进行神经功能缺损评分。结果血肿周围脑组织HO-1在6h即开始表达，24h明显增多，48-72h达高峰；脑组织含水量在24h无明显变化，48h有所增加，72h显著增加并达到高峰，随后逐步下降；二者呈正相关（r=0．760，P％0．05）。ICH后各时间点神经功能缺损评分与相应时间点血肿周围脑组织HO-1表达的水平呈正相关（r=0．669，P〈0．05）。结论HO-1的表达在红细胞致ICH后迟发性脑损伤和脑水肿的形成过程中起着重要作用。

Effect of HO-1 on brain damage following experimental hemorrhage in rats

Objective To investigate the effect of heme oxygenase-1(HO-1) on brain damage following experimental hemorrhage in rats.Methods Experimental intracerebral hemorrhage model was made by injected autologous packed erythrocytes using stereotactic method.The expression of HO-1 perihematoma at different time was detected using immunohistochemitry techniques and brain water content were measured,and neurobehavioraloutcomes were assessed in the meantime.Results The expression of HO-1 appeared at 6 hours after ICH and peaked at 48~72 hours.The brain water content was not increased within 24 hour after ICH,but increased gradully at 48 hour,peaked at 72 hour,then decreased gradully;there was a positive correlation between the expression of HO-1 and the brain water content(r=0.760,P<0.05).Neurobehavioral scores at various stages after operation in ICH group were positively correlated with the expression of HO-1 respectively(r=0.669,P<0.05).Conclusions The expression of HO-1 plays an important part in delayed brain damage and brain edema following ICH.