The anti-inflammatory activity of COL-3 is reproduced by reducing oxidative stress or glucose utilization
Next, we wished to determine whether COL-3 suppressive effects on TNF-α release were reproduced by lowering ROS production or glucose utilization. In line with this possibility, we established that the NADPH inhibitor APO (300 µM) and the non-metabolizable glucose analog 2DG (500 µM) (Figure 6A) were as effective as COL-3 to reduce TNF-α release induced by LPS or αSa, thus further supporting the view that COL-3 exerts its anti-inflammatory effect by interfering with a glucose-dependent mechanism that promotes oxidative stress (Figure 6B).