白质
蛛网膜下腔出血
内科学
髓鞘
内分泌学
医学
少突胶质细胞
运输机
麻醉
化学
中枢神经系统
生物化学
磁共振成像
基因
放射科
作者
Xin Wu,Zongqi Wang,Haiying Li,Xing Xie,Jiang Wu,Haitao Shen,Xiang Li,Zhong Wang,Gang Chen
标识
DOI:10.1007/s11684-021-0879-9
摘要
Monocarboxylic acid transporter 1 (MCT1) maintains axonal function by transferring lactic acid from oligodendrocytes to axons. Subarachnoid hemorrhage (SAH) induces white matter injury, but the involvement of MCT1 is unclear. In this study, the SAH model of adult male Sprague-Dawley rats was used to explore the role of MCT1 in white matter injury after SAH. At 48 h after SAH, oligodendrocyte MCT1 was significantly reduced, and the exogenous overexpression of MCT1 significantly improved white matter integrity and long-term cognitive function. Motor training after SAH significantly increased the number of ITPR2+SOX10+ oligodendrocytes and upregulated the level of MCT1, which was positively correlated with the behavioral ability of rats. In addition, miR-29b and miR-124 levels were significantly increased in SAH rats compared with non-SAH rats. Further intervention experiments showed that miR-29b and miR-124 could negatively regulate the level of MCT1. This study confirmed that the loss of MCT1 may be one of the mechanisms of white matter damage after SAH and may be caused by the negative regulation of miR-29b and miR-124. MCT1 may be involved in the neurological improvement of rehabilitation training after SAH.
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