Diphlorethohydroxycarmalol Attenuates Methylglyoxal-Induced Oxidative Stress and Advanced Glycation End Product Formation in Human Kidney Cells

Figure 8

Possible mechanisms for the inhibition of AGE accumulation by DPHC in MGO-treated HEK cells. DPHC promotes the expression of not only antioxidant and phase II detoxifying enzymes but also Glo-1 by mediating Nrf2 activation. This inhibits oxidative stress and formation of AGEs, effectively attenuating cell damage. DPHC: diphlorethohydroxycarmalol; MGO: methylglyoxal; Nrf2: nuclear factor erythroid 2-related factor 2; ARE: antioxidant response element; ROS: reactive oxygen species; AGEs: advanced glycation end products; Glo-1: glyoxalase 1; SOD: superoxide dismutase; CAT: catalase; HO-1: heme oxygenase-1; NQO: NAD(P)H quinone dehydrogenase 1; GCL: γ-glutamylcysteine synthetases.