中国神经再生研究(英文版) ›› 2022, Vol. 17 ›› Issue (6): 1261-1262.doi: 10.4103/1673-5374.327339

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

早产新生儿脑损伤:人羊膜上皮干细胞是否可以作为神经保护和神经修复的泛疗法吗?

  

  • 出版日期:2022-06-15 发布日期:2021-12-17

Preterm neonatal brain injury: are human amnion epithelial stem cells a pan-treatment for neuroprotection and neurorepair?

Joanne O. Davidson, Simerdeep K. Dhillon, Laura Bennet*   

  1. Department of Physiology, University of Auckland, Auckland, New Zealand
  • Online:2022-06-15 Published:2021-12-17
  • Contact: Laura Bennet, PhD, l.bennet@auckland.ac.nz.
  • Supported by:
    The present study was supported by the Health Research Council of New Zealand (17/601, 12/613) (to LB). 

摘要: Neural Regen Res:人羊膜上皮细胞的神经修复和神经保护
    尽管随着医学技术的发展早产儿的死亡率已稳步下降,但神经发育障碍率仍然很高,包括严重的运动障碍,如脑瘫。目前没有针对早产脑损伤或神经发育受损的标准临床神经保护治疗。鉴于病因是多因素的,并且本质上可能具有协同作用,因此开发治疗方法是一项重大挑战。早产本身是潜在不利的产前和产后因素(包括急性和/或慢性缺氧和炎症)与临床治疗(如产前类固醇)、产后心肺功能受损、通气、感染和正在进行的临床药物治疗(包括抗惊厥药、镇痛药和产后皮质类固醇。使这一点更加复杂的是损伤对神经成熟阶段的影响,导致更严重的神经发育受损。人羊膜上皮细胞可以很容易地从胎盘羊膜中提取,易于快速治疗。前期研究表明人羊膜上皮细胞是多能的,能够分化为所有三个胚层的细胞类型,是非致瘤性和非免疫原性的。人羊膜上皮细胞具有显著的免疫调节特性,包括增加抗炎细胞因子和减少促炎细胞因子以及增加神经营养因子的释放,包括脑源性神经营养因子、神经胶质源性神经营养因子和神经营养因子-3,这些使它们成为理想的疗法。
    来自新西兰奥克兰大学的Laura Bennet团队认为,即使治疗延迟(至少 24 小时),人羊膜上皮细胞早产新生儿具有保护作用。需要进一步的大量工作来确定最佳剂量以及多次剂量的给药方案。
    文章在《中国神经再生研究(英文版)》杂志2022年 6 月  6 期发表。

Abstract: Premature birth, defined as birth before 37 weeks completed gestation, represents 11.1% of all live births worldwide and the rate has increased in almost all countries over the past few decades (Dhillon et al., 2018). Although mortality after preterm birth has fallen steadily over time, preterm infants continue to have very high rates of neurodevelopmental disability, including severe motor disorders such as cerebral palsy (Dhillon et al., 2018; Yates et al., 2021). Currently there are no standard clinical neuroprotection treatments for preterm brain injury or impaired neurodevelopment. Development of treatments is a significant challenge given that the etiology is multifactorial and potentially synergistic in nature. Preterm birth itself acts as an intersect between potential adverse antenatal and postnatal factors including acute and/or chronic hypoxia and inflammation and clinical treatments such as antenatal steroids, with post-natal cardio-respiratory compromise, ventilation, infection, and ongoing clinical drug treatments including anticonvulsants, analgesics and postnatal corticosteroids (Bennet et al., 2018; Dhillon et al., 2018; Yates et al., 2021). Compounding this is the impact of injury on the stage of neural maturation leading to greater impaired neurodevelopment (Dhillon et al., 2018; Yates et al., 2021).