Open AccessHuman umbilical cord-derived mesenchymal stem cells promote repair of neonatal brain injury caused by hypoxia/ischemia in rats
Author(s) -
Wei Zou,
Jing Liu,
Yang Jiao,
Yue-Tong Sun,
Nai-Fei Chen,
Lanlan Zhou,
Xin Guan,
Jiayi Wang,
Wenjuan Wei,
Chao Han,
Xiaoyu Jiang,
Ya-Chen Wang
Publication year - 2022
Publication title -
neural regeneration research/neural regeneration research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.339002
Subject(s) - umbilical cord , mesenchymal stem cell , medicine , glial fibrillary acidic protein , hypoxia (environmental) , lipopolysaccharide , astrocyte , ischemia , immune system , immunology , chorioamnionitis , brain damage , pathology , fetus , central nervous system , pregnancy , biology , immunohistochemistry , chemistry , organic chemistry , oxygen , genetics
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.