Fig. 3

Hippocampal hyperglycemia contributes to CUMS-induced microglial proinflammatory activation. (A) Glucose levels in hippocampus lysates from CTRL and CUMS mice (n = 6, Student’s t-test). (B) Representative PET images of ¹⁸F-FDG uptake in the hippocampus in CTRL and CUMS mice (left) and the quantified result (right) (n = 5, Student’s t-test). (C) Correlation between glucose levels and IL-6, IL-1β, and TNF-α levels in the hippocampus (n = 12, Pearson’s correlation analysis). (D) Schematic of glucose infusion into the hippocampus and experimental timeline. Mice infused with saline were used as a control. (E) qRT-PCR assays monitoring the expression of proinflammatory phenotype markers, CD86, IL-6, IL-1β, and TNF-α in hippocampal samples from glucose-infused and control mice (n = 6, Student’s t-test). (F) Levels of IL-6, IL-1β, and TNF-α in hippocampus lysates from glucose-infused and control mice as determined by ELISA (n = 4, Student’s t-test). *p < 0.05, **p < 0.01