补体在大鼠脑缺血-再灌注损伤中的作用

目的观察补体C1q和C3d在大鼠脑缺血-再灌注损伤过程中表达水平的动态变化，探讨其与脑水肿、脑损伤的相关性和作用机制。方法采用线栓法制备大鼠大脑中动脉闭塞(MCAO)模型，缺血2h后再灌注。应用免疫组化法检测脑内补体C1q和C3d蛋白的表达，记录大脑神经功能缺失程度、脑组织含水量的动态变化。结果局灶性脑缺血-再灌注损伤后脑内补体C1q和C3d蛋白的表达水平逐渐增加，至缺血-再灌注后24h达高峰，至再灌注后120h左右恢复至正常水平。脑组织含水量在缺血-再灌注24～72h达高峰。神经功能缺失最重的时间点出现在缺血-再灌注后24h。补体C1q和C3d的表达水平与脑水肿和神经功能缺失呈正相关。结论脑缺血-再灌注后补体激活参与其损伤过程，抑制补体激活有望成为新的治疗脑缺血-再灌注损伤的靶点。

The role of complement during rat cerebral ischemia-reperfusion injury

Objective To investigate dynamic changes of complement (C1q and C3d) expression during cerebral ischemia-reperfusion injury and its correlation with brain injury , and to discuss its possible mechanisms. Methods The middle cerebral artery occlusion (MACO) model was induced through filament method. Immunohistochemical method was used to detect complement (C1q and C3d)expression. The dynamic changes of neurological deficit scores and brain water content was recorded. Results The complement (C1q and C3d) expression increased gradually after local cerebral ischemia-reperfusion injury, peaked at 24h after ischemia-reperfusion ,and returned to normal at 120h after reperfusion. Brain water content was highest at 24 to 72 h after reperfusion. The time point of the most severest neurological deficit was at 24 h after reperfusion. The complement (C1q and C3d)expression was positively correlated with brain edema and neurological deficit. Conclusions The activation of complement may participate in the course of the injury after ischemia-reperfusion, so inhibition of complement is likely to be the target of treatment.