Chen Andi, Chen Xiaohui, Deng Jianhui, Zheng Xiaochun
Department of Anesthesiology, Shengli Clinical Medical College of Fujian Medical University, Fujian Provincial Hospital, Fuzhou, China.
Fujian Emergency Medical Center, Fujian Provincial Key Laboratory of Emergency Medicine, Fujian Provincial Key Laboratory of Critical Care Medicine, Fujian Provincial Co-Constructed Laboratory of "Belt and Road", Fuzhou, China.
Front Pediatr. 2022 Oct 10;10:986452. doi: 10.3389/fped.2022.986452. eCollection 2022.
Hypoxic-ischemic brain damage (HIBD) is the main cause of perinatal mortality and neurologic complications in neonates, but it remains difficult to cure due to scarce treatments and complex molecular mechanisms remaining incompletely explained. Recent, mounting evidence shows that endogenous neurogenesis can improve neonatal neurological dysfunction post-HIBD. However, the capacity for spontaneous endogenous neurogenesis is limited and insufficient for replacing neurons lost to brain damage. Therefore, it is of great clinical value and social significance to seek therapeutic techniques that promote endogenous neurogenesis, to reduce neonatal neurological dysfunction from HIBD. This review summarizes the known neuroprotective effects of, and treatments targeting, endogenous neurogenesis following neonatal HIBD, to provide available targets and directions and a theoretical basis for the treatment of neonatal neurological dysfunction from HIBD.
缺氧缺血性脑损伤（HIBD）是新生儿围产期死亡和神经并发症的主要原因，但由于治疗方法匮乏且复杂的分子机制仍未完全阐明，其治疗仍很困难。最近，越来越多的证据表明，内源性神经发生可以改善HIBD后新生儿的神经功能障碍。然而，内源性神经发生的自发能力有限，不足以替代因脑损伤而丢失的神经元。因此，寻找促进内源性神经发生的治疗技术，以减少HIBD导致的新生儿神经功能障碍，具有重要的临床价值和社会意义。本文综述了新生儿HIBD后内源性神经发生的已知神经保护作用及针对其的治疗方法，为HIBD所致新生儿神经功能障碍的治疗提供可用的靶点、方向和理论依据。
