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. 2020 Jul 19;21(14):5104. doi: 10.3390/ijms21145104

Figure 1.

Figure 1

Inhibition of Cbl increased the glycolytic capacity and mitochondrial respiration. (A) Immunoblot of Cbl and nod-like receptor 3 (NLRP3) inflammasome molecules in wild-type (WT) and Cbl-knockout (KO) THP-1-derived macrophages; (B) extracellular acidification rate (ECAR) of WT and Cbl-KO THP-1-derived macrophages; (C) WT and Cbl-KO HEK293T cells; and (D) hydrocotarnine-treated and untreated THP-1-derived macrophages, under sequential treatment (dotted vertical lines) with glucose, oligomycin (Oligo), and 2-deoxyglucose (2DG). The glycolytic capacity and glycolytic reserve capacity are calculated in the right panels. (E) Oxygen consumption rate (OCR) of Cbl-KO THP-1-derived macrophages; (F) Cbl-KO HEK293T cells; and (G) hydrocotarnine-treated THP-1-derived macrophages, under sequential treatment (dotted vertical lines) with oligomycin, carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP), and rotenone plus antimycin. Maximum respiration and spare respiratory capacity (SRC) are calculated in the right panels. * p < 0.05; ** p < 0.01. All results are presented as the mean ± standard deviation (SD) of the three independent experiments and were analyzed using the Student’s t-test.