7-O-galloyl-D-sedoheptulose attenuates oxidative stress-induced diabetic injury via decreasing expression of nuclear factor-κB- and apoptosis-related protein in the liver.

The present study was conducted to examine whether 7-O-galloyl-D-sedoheptulose (GS) has an ameliorative effect on diabetic alterations such as oxidative stress, inflammation, and apoptosis in the liver of type 2 diabetic db/db mice. GS was administered at 20 or 100 mg/kg body weight per day for 6 weeks to db/db mice, and its effect was compared with vehicle-treated db/db and m/m mice. In the serum and hepatic tissue, biochemical factors and protein expressions associated with nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, inflammation, and apoptosis were examined. As a result, GS administration to type 2 diabetic mice lowered serum and hepatic oxidative stress through the reduction of reactive oxygen species and lipid peroxidation. These results were derived, at least in part, from attenuating the expression of NADPH oxidase subunit proteins, Nox-4 and p22(phox). In the diabetic condition, augmented nuclear factor (NF)-E2-related factor 2 and heme oxygenase-1 were reduced with a decrease in oxidative stress on GS treatment. Furthermore, in the GS-treated group, NF-kappa B-related pro-inflammatory factors and pro-apoptotic protein expressions were alleviated in the hepatic tissue. Taking these into consideration, our findings support the therapeutic evidence for GS ameliorating the development of diabetic complications via regulating oxidative stress, inflammation, and apoptosis.