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Fig. 3 | Journal of Neuroinflammation

Fig. 3

From: Early glycolytic reprogramming controls microglial inflammatory activation

Fig. 3

Glycolytic inhibitors suppress the inflammatory response by negatively regulating NF-κB signaling pathways. a BV-2 microglial cells stably expressing NF-κB luciferase reporter construct were pretreated with 2-DG (600–1000 μM) for 30 min, followed by LPS (200 ng/mL) stimulation for 16 h. The transcriptional activity of NF-κB was determined by luciferase reporter assay. b BV-2 microglial cells were pretreated with 2-DG for 30 min, followed by treatment of lipopolysaccharide (LPS)-Alexa Fluor® 488 for 2 h. The binding efficiency was analyzed using flow cytometry. c HEK293T cells stably expressing NF-κB luciferase reporter construct were transfected with indicated plasmid. After a 16-h transfection, the cells were treated with 2-DG for 8 h. The NF-κB transcriptional activity was determined by luciferase reporter assay. d BV-2 microglial cells were pretreated with 2-DG (1000 μM) for 30 min, followed by LPS (200 ng/mL) treatment for 30 min. The expression of p-JNK, JNK, p-ERK, ERK, p-p38, and p38 was detected by Western blotting (left), and the relative protein levels were quantified by densitometric analysis (right). e BV-2 microglial cells were treated with 2-DG (1000 μM) for 30 min prior to LPS stimulation for 30 min. The expression of p-TBK1 was analyzed by Western blotting (upper), and the relative protein levels were quantified by densitometric analysis (lower). Data are presented as mean ± S.D. (n=3) and are representative of results obtained from three independent experiments. *p < 0.05, **p <0.01 compared to the LPS alone group or control group

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