Fig. 6

Glucose-mediates the proinflammatory activation of BV2 cells through GLUT1. (A) qRT-PCR assays monitoring expression of proinflammatory phenotype markers, CD86, IL-6, IL-1β, and TNF-α in LV-GFP- or LV-GLUT1-infected BV2 cells with or without glucose treatment (n = 6, One-way ANOVA with Tukey’s post hoc test). (B) Flow cytometry analysis of CD86⁺ populations in BV2-LV-GFP/LV-GLUT1 cells under control or glucose conditions. Representative images (left); quantified result (right, n = 5, One-way ANOVA with Tukey’s post hoc test). (C) Levels of secreted IL-6, IL-1β, and TNF-α proteins in the supernatant of BV2-LV-GFP/LV-GLUT1 cells with or without glucose treatment (n = 6, One-way ANOVA with Tukey’s post hoc test). (D) qRT-PCR assays evaluating the expression of proinflammatory phenotype markers, CD86, IL-6, IL-1β and TNF-α in BV2 cells exposed to GLUT1 inhibitors (STF-31, 5 µmol/L and BAY-876, 50 nmol/L) for 48 h with or without glucose treatment (n = 6, One-way ANOVA with Tukey’s post hoc test). (E) Flow cytometry analysis of CD86⁺ populations in BV2 cells exposed to STF-31 or BAY-876 under control or glucose conditions. Representative images (left); quantified result (right, n = 5, One-way ANOVA with Tukey’s post hoc test). (F) Levels of secreted IL-6, IL-1β and TNF-α proteins in the supernatant of BV2 cells exposed to STF-31 or BAY-876 with or without glucose treatment (n = 6, One-way ANOVA with Tukey’s post hoc test). *p < 0.05, **p < 0.01