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首页> 外文期刊>Experimental and therapeutic medicine >Pretreatment with human urine-derived stem cells protects neurological function in rats following cardiopulmonary resuscitation after cardiac arrest
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Pretreatment with human urine-derived stem cells protects neurological function in rats following cardiopulmonary resuscitation after cardiac arrest

机译:与人尿衍生的干细胞进行预处理保护心脏骤停后心肺复苏后大鼠的神经功能

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摘要

Cardiopulmonary resuscitation (CPR) after cardiac arrest (CA) often leads to neurological deficits in the absence of effective treatment. The aim of the present basic research study was to investigate the effects of human urine-derived stem cells (hUSCs) on the recovery of neurological function in rats after CA/CPR. hUSCs were isolated in vitro and identified using flow cytometry. A rat model of CA was established, and CPR was performed. Animals were scored for neurofunctional deficits following hUSC transplantation. The expression levels of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) in the hippocampus and temporal cortex were detected via immunofluorescence. Moreover, brain water content and serum S100 calcium binding protein B (S100B) levels were measured 7 days following hUSC transplantation. The results demonstrated that hUSCs had upregulated expression levels of CD29, CD90, CD44, CD105, CD73, CD224 and CD146, and expressed low levels of CD34 and human leukocyte antigen-DR isotype. In addition, hUSCs were able to differentiate into neuronal cells in vitro. The SPSS 19.0 statistical package was used for statistical analysis, and it was found that the neurological function of the rats after CA/CPR was significantly improved following hUSC transplantation. Furthermore, hUSCs aggregated in the hippocampus and temporal cortex, and secreted large amounts of BDNF and VEGF. hUSC transplantation also effectively inhibited brain edema and serum S100B levels after CPR. Therefore, the results suggested that hUSC transplantation significantly improved the neurological function of rats after CA/CPR, possibly by promoting the expression levels of BDNF and VEGF, as well as inhibiting brain edema.
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