膜攻击复合物抑制剂 CD59a 可保护小鼠免受局灶性脑缺血的影响。

BACKGROUND

The complement system is a crucial mediator of inflammation and cell lysis after cerebral ischemia. However, there is little information about the exact contribution of the membrane attack complex (MAC) and its inhibitor-protein CD59.

METHODS

Transient focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in young male and female CD59a knockout and wild-type mice. Two models of MCAO were applied: 60 min MCAO and 48 h reperfusion, as well as 30 min MCAO and 72 h reperfusion. CD59a knockout animals were compared to wild-type animals in terms of infarct size, edema, neurological deficit, and cell death.

RESULTS AND DISCUSSION

CD59a-deficiency in male mice caused significantly increased infarct volumes and brain swelling when compared to wild-type mice at 72 h after 30 min-occlusion time, whereas no significant difference was observed after 1 h-MCAO. Moreover, CD59a-deficient mice had impaired neurological function when compared to wild-type mice after 30 min MCAO.

CONCLUSION

We conclude that CD59a protects against ischemic brain damage, but depending on the gender and the stroke model used.

背景

补体系统是脑缺血后炎症和细胞溶解的关键介质。然而，关于膜攻击复合物（MAC）及其抑制剂蛋白 CD59 的确切作用知之甚少。

方法

通过大脑中动脉闭塞（MCAO）在年轻雄性和雌性 CD59a 敲除和野生型小鼠中诱导短暂性局灶性脑缺血。应用了两种 MCAO 模型：60 分钟 MCAO 和 48 小时再灌注，以及 30 分钟 MCAO 和 72 小时再灌注。在梗死体积、水肿、神经功能缺损和细胞死亡方面，将 CD59a 敲除动物与野生型动物进行比较。