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目的:探讨补体受体2型(Complement Receptortype2,CR2)在实验性脑梗死(cerebral infarction,CI)后继发性脑损伤中的作用。方法:应用实验性大鼠大脑中动脉梗死模型(middlecerebral artery occlusion,MCAO),于术后6h、24h、48h、72h和7d采用Longa评分法、肢体对称试验评分法、Berderson评分法和平衡木评分法等4种方法进行行为学评分;用免疫组化染色观察炎性细胞浸润;用单克隆CR2抗体检测病灶周围脑组织CR2表达。结果:大鼠脑梗死后脑水肿、炎性细胞浸润均于48h达到高峰,CR2的表达高峰在术后6h即有表达,24h～72h达高峰,至7d仍有表达,CR2表达与脑梗死后脑水肿及脑损伤存在时间上相关,且与对照组相比有统计学意义,P<0.05。结论:CR2在脑梗死后脑组织损伤和脑水肿的形成中起到了一定的作用。
Objective: To investigate the role of Complement Receptortype 2 (CR2) in secondary brain injury following experimental cerebral infarction (CI). Methods: The middle cerebral artery occlusion (MCAO) was used in rats. The Longa score, limb symmetry test score, Berderson score and balance beam score method were used at 6h, 24h, 48h, 72h and 7d after operation. And other four methods for behavioral scoring; inflammatory cell infiltration was observed by immunohistochemical staining; CR2 expression in brain tissue around the lesion was detected by monoclonal CR2 antibody. Results: Cerebral edema and infiltration of inflammatory cells peaked at 48h after cerebral infarction in rats. The expression peak of CR2 reached its peak at 6h after operation and peaked at 24h to 72h. The expression of CR2 remained at 7d, and the expression of CR2 correlated with cerebral edema And brain damage were related in time, and compared with the control group was statistically significant, P <0.05. CONCLUSION: CR2 plays a role in the formation of brain injury and cerebral edema after cerebral infarction.