The role of complement C3 in intracerebral hemorrhage-induced brain injury
The role of complement C3 in intracerebral hemorrhage-induced brain injury
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DOI：
10.1038/sj.jcbfm.9600305
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发表时间：
2006-12-01
影响因子：
6.3
通讯作者：
Xi, Guohua
中科院分区：
文献类型：
--
作者：
Yang, Shuxu;Nakamura, Takehiro;Xi, Guohua
脑出血(ICH)后补体级联反应的激活与脑损伤密切相关。然而，最近的一项研究发现，补体C5缺乏的小鼠加重了脑出血引起的脑损伤。因此，本研究调查了补体C3(位于C5的上游)在脑出血中的作用。雄性补体C3缺乏而补体充足的小鼠脑内输注30亩L自体全血。处死小鼠，取脑组织进行水肿、Western blotting、免疫组织化学和组织学分析。并于脑出血前后进行前肢使用、不对称试验、转弯等行为学测试。与补体C3充足的小鼠相比，补体C3缺乏的小鼠脑出血后脑水肿减轻，血红素氧合酶-1水平降低，小胶质细胞活化减少，血栓周围中性粒细胞浸润减少。此外，与C3充足的小鼠相比，C3缺乏的小鼠较少出现脑出血诱导的前肢使用不对称缺陷。提示补体激活可能影响脑出血后的血红素代谢和炎症反应，提示补体C3是导致脑出血后脑损伤的重要因素。
Activation of the complement cascade contributes to brain injury after intracerebral hemorrhage (ICH). However, a recent study found that complement C5 deficient mice had enhanced ICH-induced brain injury. The present study, therefore, investigated the role of complement C3 (which is upstream from C5) in ICH. Male complement C3 deficient and sufficient mice had an intracerebral infusion of 30-mu L autologous whole blood. The mice were killed and the brains were sampled for edema, Western blotting, immunohistochemistry and histologic analysis. Behavioral tests including forelimb use asymmetry test and corner turn were also performed before and after ICH. Compared to complement C3 sufficient mice, C3 deficient mice had less brain edema, lower hemeoxygenase-1 levels, less microglia activation and neutrophil infiltration around the clot after ICH. In addition, the C3-deficient mice had less ICH-induced forelimb use asymmetry deficits compared with C3-sufficient mice. These results suggest complement activation may affect heme metabolism and the inflammatory response after ICH suggesting that complement C3 is an important factor causing ICH-induced brain injury.