Perinatal hypoxic-ischemic (HI) brain injury is the major cause of neonatal mortality and severe long-term neurological morbidity. Yet, the effective therapeutic interventions currently available are extremely limited. Corticosteroids act on both mineralocorticoid (MR) and glucocorticoid (GR) receptors and modulate inflammation and apoptosis in the brain. Neuroinflammatory response to acute cerebral HI is a major contributor to the pathophysiology of perinatal brain injury. Here, we give an overview of current knowledge of corticosteroid-mediated modulations of inflammation and apoptosis in the neonatal brain, focusing on key regulatory cells of the innate and adaptive immune response. In addition, we provide new insights into targets of MR and GR in potential therapeutic strategies that could be beneficial for the treatment of infants with HI brain injury.

围产期缺氧缺血性脑损伤是新生儿死亡和严重的长期神经系统疾病的主要原因。然而，当前可用的有效治疗干预措施是极其有限的。皮质类固醇同时作用于盐皮质激素（MR）和糖皮质激素（GR）受体，并调节大脑的炎症和细胞凋亡。对急性脑HI的神经炎症反应是围产期脑损伤的病理生理学的主要贡献者。在这里，我们概述了皮质类固醇介导的新生儿大脑炎症和细胞凋亡的调制的当前知识，重点是先天性和适应性免疫反应的关键调节细胞。此外，