Bao X, Wu G, Hu S, Huang F
Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China.
Acta Neurochir Suppl. 2008;105:23-7. doi: 10.1007/978-3-211-09469-3_5.
Brain edema induced by intracerebral hemorrhage (ICH) is a serious problem in the treatment of ICH. However, the mechanisms of brain edema formation following ICH are not well-understood. We have found that hemoglobin plays an important role in edema development after ICH. In this study, we sought to explore the mechanism of brain edema formation caused by hemoglobin. Hemoglobin was infused into the right basal ganglia of male Sprague-Dawley rats. The animals were killed 24h later to detect brain water and ion content. Meanwhile, Western blot analysis and immunohistochemical studies were applied for Poly(ADP-ribose) polymerase (PARP) measurement. The effect of the iron chelator, deferoxamine, on PARP activation was also examined. We found that intracerebral infusion of hemoglobin caused an increase in brain water content at 24h. At the same time, PARP was activated after hemoglobin infusion. Deferoxamine (500 mg/kg, i.p.) reduced hemoglobin-induced brain edema and activation of PARP. These results demonstrate that hemoglobin can cause brain edema and activate PARP in rat brain.
脑出血（ICH）所致脑水肿是脑出血治疗中的一个严重问题。然而，脑出血后脑水肿形成的机制尚未完全明确。我们发现血红蛋白在脑出血后水肿发展过程中起重要作用。在本研究中，我们试图探究血红蛋白引起脑水肿形成的机制。将血红蛋白注入雄性Sprague-Dawley大鼠的右侧基底神经节。24小时后处死动物以检测脑含水量和离子含量。同时，采用蛋白质免疫印迹分析和免疫组化研究检测聚（ADP-核糖）聚合酶（PARP）。还研究了铁螯合剂去铁胺对PARP激活的影响。我们发现脑内注入血红蛋白在24小时时导致脑含水量增加。同时，血红蛋白注入后PARP被激活。去铁胺（500mg/kg，腹腔注射）减轻了血红蛋白诱导的脑水肿和PARP激活。这些结果表明血红蛋白可导致大鼠脑水肿并激活PARP。
