Fluoxetine increases astrocytic glucose uptake and glycolysis in corticosterone-induced depression through restricting GR-TXNIP-GLUT1 Pathway

被引:13
作者
Pan, Shu-Man [1 ]
Zhou, Yi-Fan [1 ]
Zuo, Na [1 ]
Jiao, Rui-Qing [1 ]
Kong, Ling-Dong [1 ,2 ]
Pan, Ying [1 ,2 ]
机构
[1] Nanjing Univ, Sch Life Sci, State Key Lab Pharmaceut Biotechnol, Nanjing, Jiangsu, Peoples R China
[2] China Pharmaceut Univ, State Key Lab Nat Med, Nanjing, Jiangsu, Peoples R China
基金
国家重点研发计划;
关键词
fluoxetine; astrocyte; glycolysis; GR; TXNIP-GLUT1; pathway; THIOREDOXIN-INTERACTING PROTEIN; PREFRONTAL CORTEX; NLRP3; INFLAMMASOME; CUMS RATS; BRAIN; ACTIVATION; STRESS; SULFORHODAMINE-101; GLUCOCORTICOIDS; METABOLISM;
D O I
10.3389/fphar.2022.872375
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Antidepressant fluoxetine can affect cerebral glucose metabolism in clinic, but the underlying molecular mechanism remains poorly understood. Here, we examined the effect of fluoxetine on brain regional glucose metabolism in a rat model of depression induced by repeated corticosterone injection, and explored the molecular mechanism. Fluoxetine was found to recover the decrease of F-18-fluorodeoxyglucose (F-18-FDG) signal in prefrontal cortex (PFC), and increased 2-[N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl) amino]-2-deoxy-D-glucose (2-NBDG, a fluorescent glucose analog) uptake in an astrocyte-specific manner in ex vivo cultured PFC slices from corticosterone-induced depressive rats, which were consistent with its improvement of animal depressive behaviors. Furthermore, fluoxetine restricted nuclear translocation of glucocorticoid receptor (GR) to suppress the transcription of thioredoxin interacting protein (TXNIP). Subsequently, it promoted glucose transporter 1 (GLUT1)-mediated glucose uptake and glycolysis of PFC astrocytes through suppressing TXNIP expression under corticosterone-induced depressive state. More importantly, fluoxetine could improve glucose metabolism of corticosterone-stimulated astrocytes via TXNIP-GLUT1 pathway. These results demonstrated that fluoxetine increased astrocytic glucose uptake and glycolysis in corticosterone-induced depression via restricting GR-TXNIP-GLUT1 pathway. The modulation of astrocytic glucose metabolism by fluoxetine was suggested as a novel mechanism of its antidepressant action.
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页数:17
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