Brain damage after hypoxia-ischemia (HI) occurs in an age-dependent manner. Neuroprotective strategies assumed to be effective in adults might have deleterious effects in the immature brain. In order to create effective therapies, the complex pathophysiology of HI in the developing brain requires exploring new mechanisms. Critical determinants of neuronal survival after HI are the extent of vascular dysfunction, inflammation, and oxidative stress, followed later by tissue repair. The key enzyme of these processes in the human body is arginase (ARG) that acts via the bioavailability of nitric oxide, and the synthesis of polyamines and proline. ARG is expressed throughout the brain in different cells. However, little is known about the effect of ARG in pathophysiological states of the brain, especially hypoxia-ischemia. Here, we summarize the role of ARG during neurodevelopment as well as in various brain pathologies.

中文翻译：

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新生儿脑缺氧缺血中的精氨酸酶途径。

缺氧缺血（HI）后的脑损伤以年龄依赖性发生。假定对成年人有效的神经保护策略可能会对未成熟的大脑产生有害影响。为了创建有效的疗法，大脑发育中的HI复杂的病理生理需要探索新的机制。HI后神经元存活的关键决定因素是血管功能障碍，炎症和氧化应激的程度，随后是组织修复。这些过程在人体中的关键酶是精氨酸酶（ARG），其通过一氧化氮的生物利用度以及多胺和脯氨酸的合成起作用。ARG在大脑中的不同细胞中表达。但是，关于ARG对大脑病理生理状态（尤其是缺氧缺血）的影响知之甚少。这里，