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目的:探讨补体受体2型在实验性大鼠脑出血后继发性脑损伤及脑水肿中的作用。方法:实验于2003-07/2004-10在河北医科大学第二医院神经内科实验室进行。60只SD大鼠随机分为脑出血后6,24,48,72h,7d及假手术6组。应用脑立体定向技术建立大鼠中等量(50μL)自体动脉血脑出血模型,分别对脑出血组及假手术组大鼠进行动态行为学评分,观察脑损伤程度;用干-湿重法行脑含水量测定;用免疫组织化学染色观察炎性细胞浸润;用单克隆补体受体2型抗体检测病灶周围脑组织补体受体2型表达。结果:大鼠脑出血后脑水肿、炎性细胞浸润均于48h达到高峰,补体受体2型的表达高峰为24～48h,即补体受体2型表达与脑水肿及脑损伤存在时间上相关,且与假手术组相比有显著性差异。结论:补体受体2型在脑出血后脑组织损伤和脑水肿的形成中起到了一定的作用,为脑细胞功能保护早期干预措施提供了实验学数据。
Objective: To investigate the role of complement receptor type 2 in secondary brain injury and cerebral edema following experimental intracerebral hemorrhage in rats. Methods: The experiment was performed at the Neurology Laboratory of the Second Hospital of Hebei Medical University from July 2003 to October 2004. Sixty SD rats were randomly divided into 6, 24, 48, 72h, 7d after cerebral hemorrhage and 6 sham operation groups. The model of middle cerebral artery occlusion (MCAO) was established by stereotactic technique in rats. The dynamic behavior score of cerebral hemorrhage and sham operation groups were respectively observed to observe the degree of brain injury. Moisture content was measured. Inflammatory cell infiltration was observed by immunohistochemical staining. Complement receptor 2 expression in brain tissue around the lesion was detected by monoclonal complement receptor type 2 antibody. RESULTS: Cerebral edema and infiltration of inflammatory cells peaked at 48h after intracerebral hemorrhage in rats. The expression of complement receptor type 2 peaked at 24-48 h. The expression of complement receptor type 2 was correlated with brain edema and brain injury in a time-dependent manner. Compared with the sham operation group, there was a significant difference. CONCLUSION: Complement receptor type 2 plays a role in the development of brain injury and cerebral edema after intracerebral hemorrhage and provides experimental data for early intervention of brain cell function protection.