Role of Antioxidants in Neonatal Hypoxic-Ischemic Brain Injury: New Therapeutic Approaches.
Role of Antioxidants in Neonatal Hypoxic-Ischemic Brain Injury: New Therapeutic Approaches.
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DOI：
10.3390/ijms18020265
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发表时间：
2017-01-28
影响因子：
5.6
通讯作者：
Hilario E
中科院分区：
文献类型：
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作者：
Arteaga O;Álvarez A;Revuelta M;Santaolalla F;Urtasun A;Hilario E
缺氧缺血性脑损伤是一个令人担忧的健康和经济问题，尽管在新生儿护理的进步。它可以导致死亡或有害的神经系统疾病，如脑瘫，运动障碍和新生儿认知缺陷。当缺氧缺血发生时，一系列多方面的事件开始发生，最终可能导致细胞死亡。由于血液供应减少而导致的较低水平的氧增加了活性氧的产生，这导致氧化应激、较高浓度的游离胞质钙和受损的线粒体功能，从而触发凋亡途径的激活、DNA片段化和细胞死亡。这种类型的病变在新生儿中的高发病率可以部分归因于发育中的大脑特别容易受到氧化应激的影响。由于抗氧化剂可以安全地与自由基相互作用，并在重要分子受损之前终止该连锁反应，因此外源性抗氧化剂治疗可能具有减少缺氧缺血引起的细胞损伤的潜力。在这篇综述中，我们集中在抗氧化治疗对围产期缺氧缺血性脑损伤的神经保护作用，根据最新的进展。
Hypoxic–ischemic brain damage is an alarming health and economic problem in spite of the advances in neonatal care. It can cause mortality or detrimental neurological disorders such as cerebral palsy, motor impairment and cognitive deficits in neonates. When hypoxia–ischemia occurs, a multi-faceted cascade of events starts out, which can eventually cause cell death. Lower levels of oxygen due to reduced blood supply increase the production of reactive oxygen species, which leads to oxidative stress, a higher concentration of free cytosolic calcium and impaired mitochondrial function, triggering the activation of apoptotic pathways, DNA fragmentation and cell death. The high incidence of this type of lesion in newborns can be partly attributed to the fact that the developing brain is particularly vulnerable to oxidative stress. Since antioxidants can safely interact with free radicals and terminate that chain reaction before vital molecules are damaged, exogenous antioxidant therapy may have the potential to diminish cellular damage caused by hypoxia–ischemia. In this review, we focus on the neuroprotective effects of antioxidant treatments against perinatal hypoxic–ischemic brain injury, in the light of the most recent advances.