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. 2021 Sep 16;12:744826. doi: 10.3389/fphar.2021.744826

FIGURE 2.

FIGURE 2

Anlotinib inhibits PFKFB3-driven glycolysis in lung myofibroblasts. (A) Venn diagram to show the overlaps between anlotinib targets and lung fibrosis-related targets. (B) Protein-protein interaction (PPI) network of common targets between anlotinib and IPF. (C) The KEGG enrichment analysis of 74 targets of common targets. (D)The GO enrichment for each section listed. The mouse lung fibroblasts were pretreated with anlotinib (1 µM) for 3 h and then exposed to TGF-β1 (10 ng/ml) for an additional 24 h, and then the cells were lysed and lactate contents in the cellular lysates (E) and culture media (F) were determined. The data are presented as fold change relative to the levels of the untreated control group (mean ± SD, n = 3). (G) Glucose uptake detected with 2-NBDG were determined. The data are presented as fold change relative to the levels of the untreated control group (mean ± SD, n = 3). (H) Extracellular acidification rate (ECAR) was assessed. (I) Glycolysis and glycolysis capacity were quantified and shown as histograms (mean ± SD, n = 3). (J) Western blot analysis of HK2、PKM2、PFKFB3、LDHA and LDHB, β-actin was used as a loading control. (K) Quantification of HK2、PKM2、PFKFB3、LDHA and LDHB protein levels relative to β-Actin is shown (mean ± SD, n = 3). I, K, *p < 0.05, **p < 0.01, ***p < 0.001 VS TGF-β1-treated group by ANOVA.