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

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

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Geng Xue 耿雪 ¹, Wang Meng 王蒙 ¹, Leng Yunjun 冷允俊 ¹, Li Lin 李琳 ¹, Yang Haiyuan 杨海元 ¹ ², Dai Yifan 戴一凡 ¹ ², Wang Ying 王盈 ¹ ²

¹ Jiangsu Key Laboratory of Xenotransplantation, Nanjing Medical University, Nanjing, Jiangsu 211166, China
中国江苏南京南京医科大学江苏省异种移植重点实验室
² Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University. Nanjing, Jiangsu 211166, China
中国江苏南京南京医科大学心血管病转化医学协同创新中心心血管病分子干预重点实验室

https://doi.org/10.7555/JBR.35.20210107

http://www.jbr-pub.org.cn/article/doi/10.7555/JBR.35.20210107

The Journal of Biomedical Research, 30 September 2021

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.

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