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通过减轻神经炎症对mfat-1转基因小鼠急性缺氧缺血性脑损伤的保护作用。

Protective effects on acute hypoxic-ischemic brain damage in mfat-1 transgenic mice by alleviating neuroinflammation.

作者信息

Geng Xue, Wang Meng, Leng Yunjun, Li Lin, Yang Haiyuan, Dai Yifan, Wang Ying

机构信息

Jiangsu Key Laboratory of Xenotransplantation, Nanjing Medical University, Nanjing, Jiangsu 211166, China.

Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu 211166, China.

出版信息

J Biomed Res. 2021 Sep 30;35(6):474-490. doi: 10.7555/JBR.35.20210107.

DOI:10.7555/JBR.35.20210107
PMID:34744086
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8637658/
Abstract

Acute hypoxic-ischemic brain damage (HIBD) mainly occurs in adults as a result of perioperative cardiac arrest and asphyxia. The benefits of n-3 polyunsaturated fatty acids (n-3 PUFAs) in maintaining brain growth and development are well documented. However, possible protective targets and underlying mechanisms of mfat-1 mice on HIBD require further investigation. The mfat-1 transgenic mice exhibited protective effects on HIBD, as indicated by reduced infarct range and improved neurobehavioral defects. RNA-seq analysis showed that multiple pathways and targets were involved in this process, with the anti-inflammatory pathway as the most significant. This study has shown for the first time that mfat-1 has protective effects on HIBD in mice. Activation of a G protein-coupled receptor 120 (GPR120)-related anti-inflammatory pathway may be associated with perioperative and postoperative complications, thus innovating clinical intervention strategy may potentially benefit patients with HIBD.

摘要

急性缺氧缺血性脑损伤（HIBD）主要发生在成年人中，是围手术期心脏骤停和窒息的结果。n-3多不饱和脂肪酸（n-3 PUFAs）在维持脑生长发育方面的益处已有充分记录。然而，mfat-1小鼠对HIBD的可能保护靶点和潜在机制需要进一步研究。mfat-1转基因小鼠对HIBD表现出保护作用，表现为梗死范围缩小和神经行为缺陷改善。RNA测序分析表明，多个通路和靶点参与了这一过程，其中抗炎通路最为显著。本研究首次表明mfat-1对小鼠HIBD具有保护作用。G蛋白偶联受体120（GPR120）相关抗炎通路的激活可能与围手术期和术后并发症有关，因此创新临床干预策略可能对HIBD患者有潜在益处。

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