Zhang Chao, Lee Jin-Yul, Keep Richard F, Pandey Aditya, Chaudhary Neeraj, Hua Ya, Xi Guohua
Department of Neurosurgery, University of Michigan, Ann Arbor, MI, USA.
Acta Neurochir Suppl. 2013;118:157-61. doi: 10.1007/978-3-7091-1434-6_29.
Previous studies have demonstrated that erythrocyte lysis and brain iron overload contribute to early brain injury after subarachnoid hemorrhage (SAH). Activation of the complement system and formation of the membrane attack complex can result in erythrocyte lysis and might, therefore, participate in such injury. This study, therefore, examined complement activation, blood-brain barrier (BBB) disruption, and brain edema in a rat SAH model.Subarachnoid hemorrhage was induced using a modified endovascular perforation technique. Brain complement activation was determined by Western blotting and immunohistochemistry. Brain edema was measured by dry/wet weight and BBB permeability assessed by measuring brain albumin levels.We found that there was expression of the membrane attack complex and clusterin in the frontal basal cortex and clot after SAH. The protein levels of the membrane attack complex were much higher in the frontal basal cortex at 72 h after SAH than those in sham (p < 0.01). We also found that brain water content was increased (81.9 ± 1.4 vs. 79.1 ± 0.2 % in sham, p < 0.05) and BBB was disrupted (albumin content: 10,695 ± 865 vs. 4,935 ± 3,121 pixels in sham, p < 0.01) 24 h after SAH.Our results suggest that complement activation after SAH might contribute to brain edema formation and BBB disruption after SAH.
先前的研究表明，红细胞溶解和脑铁过载会导致蛛网膜下腔出血（SAH）后的早期脑损伤。补体系统的激活和膜攻击复合物的形成可导致红细胞溶解，因此可能参与此类损伤。因此，本研究在大鼠SAH模型中检测了补体激活、血脑屏障（BBB）破坏和脑水肿情况。
采用改良的血管内穿刺技术诱导蛛网膜下腔出血。通过蛋白质印迹法和免疫组织化学法测定脑补体激活情况。通过干/湿重测量脑水肿，并通过测量脑白蛋白水平评估血脑屏障通透性。
我们发现SAH后额叶基底皮质和血凝块中有膜攻击复合物和簇集素表达。SAH后72小时额叶基底皮质中膜攻击复合物的蛋白水平比假手术组高得多（p < 0.01）。我们还发现SAH后24小时脑含水量增加（假手术组为79.1±0.2%，SAH组为81.9±1.4%，p < 0.05），血脑屏障被破坏（假手术组白蛋白含量为4,935±3,121像素，SAH组为10,695±865像素，p < 0.01）。
我们的结果表明，SAH后的补体激活可能导致SAH后脑水肿形成和血脑屏障破坏。
