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. 2024 Jan 3;300(2):105620. doi: 10.1016/j.jbc.2023.105620

Figure 5.

Figure 5

SARM1 inhibits the upregulation of glycolysis in proinflammatory macrophages and alters the expression of Il1b and Il10.A–F, WT and Sarm1−/− BMDM were treated with 100 ng/ml LPS for 24 h and real-time changes in OCR and ECAR were measured by Seahorse XF analysis. Representative OCR (A) and ECAR (D) trace of seven independent experiments and each experiment was performed with six technical replicates. Dotted lines indicate injection times of mitochondrial inhibitors, oligomycin (1 μM), FCCP (1 μM), rotenone (1 μM), and antimycin A (2 μM). Basal respiration (B), maximal respiration (C), basal glycolysis (E), and glycolytic reserve (F) were calculated and displayed as scattered dot plots. Data are mean ± SEM from seven independent experiments and each experiment was performed with six technical replicates. G–I, WT and Sarm1−/− BMDM were treated with 100 ng/ml LPS for the indicated times. Expression of Il1b (G), Il6 (H), and Il10 (I) mRNA were assayed by quantitative RT-PCR and normalized to the housekeeping gene β-actin. J, WT and Sarm1−/− BMDM were stimulated with 100 ng/ml LPS for 24 h. Supernatants were assayed for IL-10 protein. Data are mean ± SEM from seven independent experiments and each experiment was performed with three technical replicates. Significance tested using two-tailed Wilcoxon matched-pairs signed-rank test; ∗p < 0.05, n.s., no significant difference. BMDM, bone marrow–derived macrophage; ECAR, extracellular acidification rate; IL, interleukin; LPS, lipopolysaccharide; OCR, oxygen consumption rate; SARM1, sterile alpha and HEAT/armadillo motif-containing protein.