Stem cell therapy for neonatal hypoxia-ischemia

干细胞治疗新生儿缺氧缺血

• 批准号: 23791229
• 负责人: ZHU Pengxiang
• 金额: $ 2.83万
• 依托单位: Ehime University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23791229/
• 关键词: 新生児医学; 脳性麻痺; 再生医学; 胚性幹細胞; 神経前駆細胞; ＥＳ細胞; 再生療法; ES細胞

Neonatal hypoxic-ischemic insult is one of the most significant cause of pediatric encephalopathy and spastic cerebral palsy. Although the developing brain's plasticity allows for remarkable self-repair, severe disruption of normal myelination and cortical development upon neonatal brain injury are likely to generate life-persisting sensory-motor and cognitive deficits in the growing child. Currently, no treatments are available that can address the long-term consequences. Thus, regenerative medicine appears as a promising avenue to help restore normal developmental processes in affected infants. Here we have demonstrated that neural stem cells derived from embryonic stem cells have shown protective effects on hypoxic-ischemic insults. Our results have suggested that stem cell therapy has proven effective in promoting functional recovery in animal models of neonatal hypoxic-ischemic injury and therefore represents a hopeful therapy for this unmet medical condition.

新生儿缺氧 - 缺血性侮辱是小儿脑病和痉挛性脑瘫的最重要原因之一。尽管发育中的大脑的可塑性允许显着自我修复，但新生儿脑损伤时正常的髓鞘形成和皮质发育的严重破坏可能会在成长中产生生命中的感觉运动和认知缺陷。目前，没有可用的治疗可以解决长期后果。因此，再生医学似乎是帮助恢复受影响婴儿正常发育过程的有前途的途径。在这里，我们证明了源自胚胎干细胞的神经干细胞对缺氧 - 缺血性损伤显示了保护作用。我们的结果表明，已证明干细胞疗法有效地促进了新生儿低氧 - 缺血性损伤动物模型的功能恢复，因此代表了这种未经治疗的医学状况的希望疗法。

项目成果

Treatment of acute spinal cord injury with intravenous infusion of a ginseng saponin, ginsenoside Rb1.

静脉滴注人参皂甙、人参皂甙Rb1治疗急性脊髓损伤。

• 发表时间: 2012
• 作者: Kimihiko Nakata;Pengxiang Zhu;Masahiro Sakanaka.
• 通讯作者: Masahiro Sakanaka.

Intravenous infusion of dihydroginsenoside Rb1 ameliorates ischemia brain damage through up-regulation of Bcl-xL and VEGF.

静脉输注二氢人参皂苷 Rb1 通过上调 Bcl-xL 和 VEGF 改善缺血性脑损伤。

• 发表时间: 2012
• 作者: Pengxiang Zhu;Kimihiko Nakata;Masahiro Sakanaka.
• 通讯作者: Masahiro Sakanaka.