Human umbilical cord-derived mesenchymal stem cells promote repair of neonatal brain injury caused by hypoxia/ischemia in rats
Autor: | Yang Jiao, Yue-Tong Sun, Nai-Fei Chen, Li-Na Zhou, Xin Guan, Jia-Yi Wang, Wen-Juan Wei, Chao Han, Xiao-Lei Jiang, Ya-Chen Wang, Wei Zou, Jing Liu |
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Jazyk: | angličtina |
Rok vydání: | 2022 |
Předmět: |
developmental brain disease model
disease-associated astrocytes intranasal administration lipopolysaccharide maternal immune activation neonatal brain injury neuroplasticity repair polypyrimidine tract-binding protein-1 stem cell therapy umbilical cord-derived mesenchymal stem cells Neurology. Diseases of the nervous system RC346-429 |
Zdroj: | Neural Regeneration Research, Vol 17, Iss 11, Pp 2518-2525 (2022) |
Druh dokumentu: | article |
ISSN: | 1673-5374 |
DOI: | 10.4103/1673-5374.339002 |
Popis: | [INLINE:1] Administration of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) is believed to be an effective method for treating neurodevelopmental disorders. In this study, we investigated the possibility of hUC-MSCs treatment of neonatal hypoxic/ischemic brain injury associated with maternal immune activation and the underlying mechanism. We established neonatal rat models of hypoxic/ischemic brain injury by exposing pregnant rats to lipopolysaccharide on day 16 or 17 of pregnancy. Rat offspring were intranasally administered hUC-MSCs on postnatal day 14. We found that polypyrimidine tract-binding protein-1 (PTBP-1) participated in the regulation of lipopolysaccharide-induced maternal immune activation, which led to neonatal hypoxic/ischemic brain injury. Intranasal delivery of hUC-MSCs inhibited PTBP-1 expression, alleviated neonatal brain injury-related inflammation, and regulated the number and function of glial fibrillary acidic protein-positive astrocytes, thereby promoting plastic regeneration of neurons and improving brain function. These findings suggest that hUC-MSCs can effectively promote the repair of neonatal hypoxic/ischemic brain injury related to maternal immune activation through inhibition of PTBP-1 expression and astrocyte activation. |
Databáze: | Directory of Open Access Journals |
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