| 马小莉,赵昕爽,蔡曙光,张昊哲,张义欢,宋明柯.天冬酰胺内肽酶和胶质细胞在创伤性脑损伤中的激活[J].,2024,(5):801-806 |
| 天冬酰胺内肽酶和胶质细胞在创伤性脑损伤中的激活 |
| Activation of the Asparaginyl Endopeptidase (AEP) and Glial Cells in a Mouse Model of Traumatic Brain Injury |
| 投稿时间：2023-11-25 修订日期：2023-12-21 |
| DOI：10.13241/j.cnki.pmb.2024.05.001 |
| 中文关键词: 创伤性脑损伤 天冬酰胺内肽酶 小胶质细胞 星形胶质细胞 神经保护 |
| 英文关键词: Traumatic Brain Injury Asparaginyl Endopeptidase Microglia Astrocytes Neuroprotection |
| 基金项目:国家自然科学基金项目（8247050413，91949116）；上海市科学技术委员会科技发展基金项目 |
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| 中文摘要: |
| 摘要 目的：创伤性脑损伤（traumatic brain injury, TBI）缺乏安全有效的治疗手段，亟须寻找新的干预靶点。天冬酰胺内肽酶 (asparaginyl endopeptidase, AEP)在免疫和神经系统疾病中起重要作用，本研究观察了小鼠TBI模型中AEP的激活和变化，探讨AEP对脑损伤和修复的意义。方法：控制性皮层撞击法在小鼠右脑半球制作TBI损伤，在造模后的不同时间点，测定受损脑组织内的乳酸含量和AEP的活性变化，免疫荧光化学染色观察TBI之后3天的胶质细胞活化，以及AEP在其中的表达。结果：TBI造成乳酸在受损脑组织内逐渐堆积，导致小胶质细胞和星形胶质细胞的反应性活化和增生，AEP的上调和激活出现在TBI的继发性脑损伤阶段，AEP在小胶质细胞和星形胶质细胞内均出现上调。结论：AEP有可能参与调控TBI引发的胶质细胞活化，在神经损伤和修复中发挥重要作用。 |
| 英文摘要: |
| ABSTRACT Objective: There is a lack of effective treatment for traumatic brain injury (TBI), and it is needed to find new intervention targets. The asparaginyl endopeptidase (AEP) plays an important role in immune and neurological diseases, and this study observed the activation and changes of AEP in a mouse TBI model to explore the significance of AEP on brain injury and repair. Methods: Controlled cortical impact was used to create TBI damage in the right cerebral hemisphere of mice, and the lactate content and AEP activity changes in the damaged brain tissue were measured at different time points after modeling, and the activation of glial cells and the expression of AEP in TBI were observed by immunofluorescence chemical staining 3 days after TBI. Results: TBI causes lactate to accumulate in damaged brain tissue, resulting in reactive activation and proliferation of microglia and astrocytes. The upregulation and activation of AEP occur in the secondary brain injury stage of TBI, and AEP is upregulated in both microglia and astrocytes. Conclusion: AEP has the potential to play an important role in nerve injury and repair by participating in the regulation of glial cell activation triggered by TBI. |
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