PDF(Pubmed)
Abstract：
Perinatal and neonatal ischemic stroke is a significant cause of cognitive and behavioral impairments. Further research is needed to support models of neonatal ischemic stroke and advance our understanding of the mechanisms of infarction formation following such strokes. We used two different levels of photothrombotic stroke (PTS) models to assess stroke outcomes in neonatal mice. We measured brain damage, dynamic changes in glial cells, and neuronal expression at various time points within two weeks following ischemic injury. Our results from 2,3,5-Triphenyltetrazolium chloride (TTC) staining and immunofluorescence staining showed that in the severe group, a dense border of astrocytes and microglia was observed within 3 days post infarct. This ultimately resulted in the formation of a permanent cortical cavity, accompanied by neuronal loss in the surrounding tissues. In the mild group, a relatively sparse arrangement of glial borders was observed 7 days post infarct. This was accompanied by intact cortical tissue and the restoration of viability in the brain tissue beyond the glial boundary. Additionally, neonatal ischemic injury leads to the altered expression of key molecules such as Aldh1L1 and Olig2 in immature astrocytes. In conclusion, we demonstrated the dynamic changes in glial cells and neuronal expression following different degrees of ischemic injury in a mouse model of PTS. These findings provide new insights for studying the cellular and molecular mechanisms underlying neuroprotection and neural regeneration after neonatal ischemic injury.
摘要：
围产期和新生儿缺血性中风是认知和行为障碍的重要原因。需要进一步的研究来支持新生儿缺血性中风的模型，并加深我们对中风后梗塞形成机制的理解。我们使用了两种不同水平的光血栓性中风（PTS）模型来评估新生小鼠的中风结局。我们测量了脑损伤，神经胶质细胞的动态变化，和神经元表达在缺血损伤后两周内的不同时间点。我们从2,3,5-氯化三苯基四唑（TTC）染色和免疫荧光染色的结果表明，在严重组，在梗死后3天内观察到星形胶质细胞和小胶质细胞的密集边界。这最终导致了永久性皮质腔的形成，伴有周围组织中的神经元损失。在温和组，梗死后7天观察到相对稀疏的神经胶质边界排列。这伴随着完整的皮质组织和超出神经胶质边界的脑组织中活力的恢复。此外,新生儿缺血性损伤导致关键分子如Aldh1L1和Olig2在未成熟星形胶质细胞中的表达改变。总之,我们证明了在PTS小鼠模型中不同程度的缺血性损伤后神经胶质细胞和神经元表达的动态变化。这些发现为研究新生儿缺血性损伤后神经保护和神经再生的细胞和分子机制提供了新的见解。
