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Fig. 4 | Arthritis Research & Therapy

Fig. 4

From: Augmented PFKFB3-mediated glycolysis by interferon-γ promotes inflammatory M1 polarization through the JAK2/STAT1 pathway in local vascular inflammation in Takayasu arteritis

Fig. 4

Effect of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) inhibition on M1 macrophage polarization and inflammatory cytokine production. AD Changes in the expression of PFKFB3, iNOS, and CD206 were detected in M1 polarization by western blot and the inhibitory effect of PFKFB3 inhibitor PFK-015 (10 μM) was examined in this process; EI expression of CD80, HLA-DR, CD163, and CD206 were detected by flow cytometry in M1 macrophage polarization, and the role of PFKFB3 was evaluated by applying its inhibitor PFK-015 (10 μM) during this process; JM levels of different cytokines (IL-1β, IL-6, IL-10, and TNF-α) were detected by ELISA in culture supernatant during M1 polarization and the role of PFKFB3 was evaluated by applying its inhibitor PFK-015 (10 μM) during this process; n = 9. LPS (50 ng/ml) was added in all the groups besides the IFN-γ (20 ng/ml) or PFK-015 (10 μM) as indicated in the figures. Data revealed as mean ± SEM, *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; #p < 0.05; ##p < 0.01; ###p < 0.001

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