静息态或M2表型的小胶质细胞主要由葡萄糖通过氧化磷酸化为细胞提供能量，病理条件下的M1促炎型小胶质细胞即使在氧气充足条件下，葡萄糖也会被优先用于糖酵解生成大量乳酸，三羧酸循环受到抑制。蛋白激酶 B（Akt）及AMP依赖的蛋白激酶（AMPK）/哺乳动物雷帕霉素靶蛋白（mTOR）/缺氧诱导因子-1α（HIF-1α）信号通路在调节糖酵解与炎症反应过程中发挥重要作用。小胶质细胞中糖酵解与炎症存在制约关系，抑制糖代谢重编程能够干预小胶质细胞 M1炎症表型极化状态，可以作为抑制神经炎症的药物作用靶点，为退行性疾病、脑血管疾病等相关药物的研发提供新思路。

Resting-state or M2 phenotype microglia are mainly energized by oxidative phosphorylation of glucose, and M1 proinflammatory microglia under pathological conditions are preferentially used for glycolysis to generate large amounts of lactate even under oxygen-sufficient conditions, and the tricarboxylic acid cycle is inhibited. The serine/threonine kinase (Akt) and AMPdependent protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/hypoxia-inducible factor-1α (HIF-1α) signaling pathway plays an important role in regulating glycolysis and inflammatory responses. Glycolysis in microglia is restricted to inflammation. Inhibition of glucose metabolism reprogramming can intervene the polarization state of M1 inflammatory phenotype in microglia, which can be used as a drug target to inhibit neuroinflammation and provide new ideas for the research and development of degenerative diseases, cerebral ischemia and other related drugs.

“十三五”期间天津市高等学校创新团队培养计划（TD13-5050）