We then evaluated the effect of BA on diabetes-mediated inflammation and found that STZ/VEH treatment significantly potentiated NFκB p65 transcriptional activity in PBMCs compared to the CTL/VEH group; BA-TOP treatment showed little effect, while treatment with either BA-IP or BA-IP/TOP partly reversed this effect (Figure 3g). This evidence concerns the gene NFKB1 and diabetes mellitus.