Carbonell T, Rama R
Department of Physiology, University of Barcelona, Avda Diagonal, 645, E-08028 Barcelona, Spain.
Curr Med Chem. 2007;14(8):857-74. doi: 10.2174/092986707780363014.
Ischemic stroke is characterized by the disruption of cerebral blood flow, which produces a central core of dead neurons surrounded by a penumbra of damaged but partially functional neurons. Many factors are associated with such brain injury, including excitotoxicity and free radicals. Recent clinical studies have shown that high plasma ferritin levels are detrimental in acute ischemic stroke. As an iron-storage protein, ferritin can act both as a scavenger and as a donor of free iron, which is a source of hydroxyl radicals. Following disruption of the blood-brain barrier, the ferritin and the free iron that have accumulated in endothelial cells in brain capillaries, together with plasma ferritin, can enter the penumbra. Iron-dependent oxidative stress in the penumbra can lead to necrosis and further neurological deterioration following ischemic stroke. An excess of iron should be considered pathological in the ischemic brain. Therapeutic strategies for ischemic stroke should attempt to restore brain function within the penumbra. Consequently, the iron content of systemic stores should be measured, and anti-oxidant treatment should be considered when it is excessive.
缺血性中风的特征是脑血流中断，这会产生一个由死亡神经元组成的中央核心，其周围是受损但仍有部分功能的神经元构成的半暗带。许多因素与这种脑损伤有关，包括兴奋性毒性和自由基。最近的临床研究表明，血浆铁蛋白水平升高在急性缺血性中风中是有害的。作为一种铁储存蛋白，铁蛋白既可以作为清除剂，也可以作为游离铁的供体，而游离铁是羟基自由基的来源。血脑屏障破坏后，积聚在脑毛细血管内皮细胞中的铁蛋白和游离铁，连同血浆铁蛋白，可进入半暗带。半暗带中铁依赖性氧化应激可导致缺血性中风后坏死和进一步的神经功能恶化。在缺血性脑中，铁过量应被视为病理性的。缺血性中风的治疗策略应试图恢复半暗带内的脑功能。因此，应测量全身储存的铁含量，当铁含量过高时应考虑抗氧化治疗。
