脑出血后的脑损伤：铁的作用
密西根大学神经外科
【摘要】
背景和目的：有证据表明，脑出血(ICH)后脑损伤部分原因是由于铁从血红蛋白中的释放。因此，我们检测是否这种铁能从脑组织中清除，以及ICH 后对可能改变铁释放和转化的蛋白质的影响：这些蛋白质包括脑血红素氧合酶-1、转铁蛋白、转铁蛋白受体和铁蛋白。我们也检测了铁在脑水肿形成、脑萎缩和神经功能缺损方面的作用。
方法：雄性斯普拉格-道利鼠，被注入100ml自体同源的全血到右侧基底神经节。增强的Perl's反应被用来铁染色，同时也检测脑非亚铁血红素的铁含量。脑血红素氧合酶-1、转铁蛋白、转铁蛋白受体和铁蛋白应用蛋白质印迹分析和免疫组织化学方法检测。采用萤光免疫双标记检验法证实哪种细胞类型表达铁蛋白。去铁胺被用做铁的螯合剂。超过实验周期，大鼠要进行行为测试(前肢放置，前肢不对称性应用和拐弯测试)。
, 百拇医药
结果：ICH引起血红素氧合酶-1的水平上调，导致脑内铁超载。4周之内，脑组织显著增高的非亚铁血红素铁没有被清除。脑转铁蛋白和转铁蛋白受体水平也增高。另外，ICH发生后，尾状核脑萎缩，伴有迟发性神经功能缺损发生。尽管随着时间流逝，部分神经功能出现恢复，但残留的神经功能缺损在3个月时仍能检测到。去铁胺能减轻脑萎缩，改善行为后果。
结论：ICH导致脑组织内铁堆积，且3个月内不能清除，促进了ICH后脑水肿的形成，脑组织损耗和神经功能缺损。铁的螯合制剂对ICH患者来说可能是有效的治疗手段。
Brain injury after intracerebral hemorrhage: the role of iron
Guohua Xi, M.D.
Department of Neurosurgery, University of Michigan
, 百拇医药
【Abstract】
Background and Purpose: Evidence indicates that brain injury after intracerebral hemorrhage (ICH) is, in part, due to the release of iron from hemoglobin. We, therefore, examined whether such iron is cleared from the brain and the effects of ICH on proteins that may alter iron release or handling: brain heme oxygenase-1, transferrin and transferrin receptor and ferritin. The role of iron in brain edema formation, brain atrophy and neurological deficits was also examined.
, http://www.100md.com
Methods: Male Sprague-Dawley rats received an infusion of 100-ml autologous whole blood into the right basal ganglia. Enhanced Perl's reaction was used for iron staining and brain non-heme iron content was also determined. Brain heme oxygenase-1, transferrin, transferrin receptor and ferritin were examined by Western blot analysis and immunohistochemistry. Immunofluorescent double labeling was performed to identify which cell types express ferritin. Deferoxamine was used as an iron chelator. Over the period of the experiment, the rats underwent behavioral testing (forelimb placing, forelimb use asymmetry and corner turn tests).
, http://www.100md.com
Results: ICH upregulated heme oxygenase-1 levels and resulted in iron overload in the brain. A marked increase in brain non-heme iron was not cleared within four weeks. Brain transferrin and transferrin receptor levels were also increased. In addition, brain atrophy in the caudate with prolonged neurological deficits occurred after ICH. Although partial functional recovery happened with time, residual neurological deficits were detectible at 3 months. Deferoxamine reduced brain atrophy and improved behavioral outcomes.
Conclusion: ICH results in an accumulation of iron in the brain that is not cleared within three months, which contributes to brain edema formation, brain tissue loss and neurological deficits after ICH. Iron chelation may be a useful therapy for ICH patients., 百拇医药
【摘要】
背景和目的：有证据表明，脑出血(ICH)后脑损伤部分原因是由于铁从血红蛋白中的释放。因此，我们检测是否这种铁能从脑组织中清除，以及ICH 后对可能改变铁释放和转化的蛋白质的影响：这些蛋白质包括脑血红素氧合酶-1、转铁蛋白、转铁蛋白受体和铁蛋白。我们也检测了铁在脑水肿形成、脑萎缩和神经功能缺损方面的作用。
方法：雄性斯普拉格-道利鼠，被注入100ml自体同源的全血到右侧基底神经节。增强的Perl's反应被用来铁染色，同时也检测脑非亚铁血红素的铁含量。脑血红素氧合酶-1、转铁蛋白、转铁蛋白受体和铁蛋白应用蛋白质印迹分析和免疫组织化学方法检测。采用萤光免疫双标记检验法证实哪种细胞类型表达铁蛋白。去铁胺被用做铁的螯合剂。超过实验周期，大鼠要进行行为测试(前肢放置，前肢不对称性应用和拐弯测试)。
, 百拇医药
结果：ICH引起血红素氧合酶-1的水平上调，导致脑内铁超载。4周之内，脑组织显著增高的非亚铁血红素铁没有被清除。脑转铁蛋白和转铁蛋白受体水平也增高。另外，ICH发生后，尾状核脑萎缩，伴有迟发性神经功能缺损发生。尽管随着时间流逝，部分神经功能出现恢复，但残留的神经功能缺损在3个月时仍能检测到。去铁胺能减轻脑萎缩，改善行为后果。
结论：ICH导致脑组织内铁堆积，且3个月内不能清除，促进了ICH后脑水肿的形成，脑组织损耗和神经功能缺损。铁的螯合制剂对ICH患者来说可能是有效的治疗手段。
Brain injury after intracerebral hemorrhage: the role of iron
Guohua Xi, M.D.
Department of Neurosurgery, University of Michigan
, 百拇医药
【Abstract】
Background and Purpose: Evidence indicates that brain injury after intracerebral hemorrhage (ICH) is, in part, due to the release of iron from hemoglobin. We, therefore, examined whether such iron is cleared from the brain and the effects of ICH on proteins that may alter iron release or handling: brain heme oxygenase-1, transferrin and transferrin receptor and ferritin. The role of iron in brain edema formation, brain atrophy and neurological deficits was also examined.
, http://www.100md.com
Methods: Male Sprague-Dawley rats received an infusion of 100-ml autologous whole blood into the right basal ganglia. Enhanced Perl's reaction was used for iron staining and brain non-heme iron content was also determined. Brain heme oxygenase-1, transferrin, transferrin receptor and ferritin were examined by Western blot analysis and immunohistochemistry. Immunofluorescent double labeling was performed to identify which cell types express ferritin. Deferoxamine was used as an iron chelator. Over the period of the experiment, the rats underwent behavioral testing (forelimb placing, forelimb use asymmetry and corner turn tests).
, http://www.100md.com
Results: ICH upregulated heme oxygenase-1 levels and resulted in iron overload in the brain. A marked increase in brain non-heme iron was not cleared within four weeks. Brain transferrin and transferrin receptor levels were also increased. In addition, brain atrophy in the caudate with prolonged neurological deficits occurred after ICH. Although partial functional recovery happened with time, residual neurological deficits were detectible at 3 months. Deferoxamine reduced brain atrophy and improved behavioral outcomes.
Conclusion: ICH results in an accumulation of iron in the brain that is not cleared within three months, which contributes to brain edema formation, brain tissue loss and neurological deficits after ICH. Iron chelation may be a useful therapy for ICH patients., 百拇医药