大鼠脑出血后血肿周围脑组织血红素氧合酶-1表达与超氧化物歧化酶活力的变化

Expression of hemeoxygenase-1 and change of superoxide dismutase activity in perihematoma after intracerebral hemorrhage in rats

目的研究脑出血(ICH)后血肿周围脑组织血红素氧合酶1(HO1)表达、抗氧化能力的变化及其相关性。方法将动物随机分为假手术(对照)组和ICH组,采用立体定向技术将自体血注入大鼠脑基底节区制作ICH动物模型,在不同时间点断头取脑,应用免疫组化法和黄嘌呤氧化法检测ICH后不同时间大鼠血肿周围脑组织HO1的表达及超氧化物歧化酶(SOD)的活力。结果ICH6h组大鼠脑组织有少量HO1阳性细胞,12～120h组HO1阳性细胞均明显增多,48h组为峰值,与对照组比较差异有极显著性(均P<0.01);168h组仍有少量表达。ICH6h组大鼠脑组织SOD活性与对照组相比差异无显著性(P>0.05);12～120h组SOD活性均明显降低,与对照组比较差异有极显著性(均P<0.01),72h组为最低值,168h组SOD活性与对照组比较差异无显著性(P>0.05)。血肿周围脑组织HO1阳性细胞数与SOD活性呈显著负相关(r=-0.878,P<0.05)。结论大鼠ICH后血肿周围脑组织HO1表达明显增加,脑组织的抗氧化能力下降。HO1可能通过氧化途径导致脑组织损伤。

Objective To study the expression of hemeoxygenase-1 （HO-1） and change of superoxide dismutase （SOD） activity in perihematoma after intracerebral hemorrhage （ICH）. Methods The rats were randomly divided into sham operating group and intracerebral hemorrhage group. Rat ICH models were induced using stereotactic infusion autologous blood 50μl into the caudate nucleus. At the due time, the rats were killed and brain tissues were removed for detection of HO-1 and t of SOD by immunohistochemical and xanthine hydroearbonylation methods. Results Following ICH, few HO-1 positive cells were observed in brain tissue perihemota at 6 h, peaked at 48 h （P 〈0.01 ） , decreased gradually and persisting until 168 h. Few HO-1 positive cells were observed in brain tissue perihemota in sham group. Compared with the sham group, SOD immunological activity in intracerebral hemorrhage group showed no statistical change at 6 h （ P 〉 0. 05 ） , then decreased gradually and reached the minimum at 72 h （ P 〈 0.01 ）. But SOD immunological activity increased gradually from that time and there was no statistical difference compared with sham group at 168 h （P 〉 0. 05 ）. The change of SOD in brain tissue perihematoma was negatively correlated with the expression of HO-1 （ r = - 0. 878, P 〈 0. 05 ）. Conclusions The expression of HO-1 perihematoma after ICH increases, while the ability of anti-oxidative decreases. The oxidative injury following ICH plays an important role in the delayed brain injury perihematoma after ICH.