补体在脑出血后脑组织损伤机制中的作用

目的研究补体C9在大鼠实验性脑出血(ICH)后血肿周围组织中的表达情况,探讨补体C9在ICH后脑水肿中的作用以及应用眼镜蛇毒因子(CVF)干预后对血肿周围组织C9表达及脑组织含水量变化的影响。方法采用立体定向技术,将自体不凝血注入大鼠尾状核制备ICH模型,将动物分为假手术组、出血组和CVF干预组,分别在不同时间断头取脑,连续切片分别作补体C9免疫组化染色和HE染色,并进行脑组织含水量测定(干湿重法)。结果ICH后2h血肿周围脑组织开始表达C9,24h达高峰。血肿周围脑组织含水量在ICH后2h开始增加(P<0.05),6h明显增加,24～72h达高峰(P<0.01),此后逐渐回落,1周基本恢复正常水平,脑组织含水量与C9的表达呈正相关关系(r=0.938,P<0.01);对侧半球相应部位及假手术对照组脑组织含水量没有明显变化;经CVF干预后,血肿周围组织C9表达明显下降,干预组与出血组之间比较有显著差异(P<0.01)。CVF干预组脑组织含水量明显低于常规ICH组(P<0.01)。结论脑出血后补体级联激活C9表达明显增加,并证明通过CVF干预后,C9表达下降,脑水肿减轻,能达到神经保护作用。

The role of completement in brain injury after intracerebral hemorrhage

Objective To investigate the expression of complement C9 after intracerebral hemorrhage (ICH) in rats, quantitate brain water contents and investigate the effect of cobra venom factor (CVF) to the expression of complement C9 and brain water contents after intracerebral hemorrhage in rats. Methods Rat ICH model was established by injecting autologous blood into the caudate nucleus of rats stereotaxically. The male rats were divided into hemorrhagic group, sham operation group and CVF treatment group. Furthermore, the hemorrhagic group was divided into several different time point groups. The complement C9 positive expression in cerebral tissues at different times was detected by using immunohistochemitry techniques. Brain edema was quantitated by wet/dry weight. Results The expression of C9 rose 2 h and peaked 48 h after ICH (P<0.01) and brain water contents in the ipsilateral basal ganglia increased slightly 2 h and peaked 24~72 h after ICH (P<0.01). There was a positive correlation between the expression of C9 and brain water contents (r=0.938, P<0.01). Administration of CVF significantly reduced the C9 expression and significantiy reduced the brain water contents in the ipsilateral basal ganglia 24~72 h after ICH. Conclusion The complement cascade may be activated after ICH. Excessive production of C9 may induce brain edema after ICH, and the expression is reduced after treatment with CVF, which could also reduce brain edema and protect the damaged brain tissue after ICH.