ABSTRACT

Monocarboxylate transporter 2 (MCT2) is the predominant monocarboxylate transporter expressed by neurons. MCT2 plays an important role in brain energy metabolism. Stroke survivors are at high risk of cognitive impairment. We reported previously that stroke-induced cognitive impairment was related to impaired energy metabolism. In the present study, we report that cognitive function was impaired after stroke in rats. We found that MCT2 expression, but not that of MCT1 or MCT4, was markedly decreased in the rat hippocampus at 7 and 28 days after transient middle cerebral artery occlusion (tMCAO). Moreover, MCT2 overexpression promoted recovery of cognitive function after stroke. The molecular mechanism underlying these effects may be related to an increase in adenosine monophosphate-activated protein kinase-mediated mitochondrial biogenesis induced by overexpression of MCT2. Our findings suggest that MCT2 activation ameliorates cognitive impairment after stroke.

摘要

单羧酸转运蛋白 2 (MCT2) 是神经元表达的主要单羧酸转运蛋白。MCT2在脑能量代谢中发挥着重要作用。中风幸存者出现认知障碍的风险很高。我们之前报道过中风引起的认知障碍与能量代谢受损有关。在本研究中，我们报告大鼠中风后认知功能受损。我们发现，在短暂性大脑中动脉闭塞（tMCAO）后7天和28天，大鼠海马中MCT2的表达显着降低，但MCT1或MCT4的表达没有显着降低。此外，MCT2过度表达促进中风后认知功能的恢复。这些作用的分子机制可能与 MCT2 过度表达诱导的单磷酸腺苷激活蛋白激酶介导的线粒体生物发生的增加有关。我们的研究结果表明 MCT2 激活可改善中风后的认知障碍。