The effect of hesperidin and quercetin on oxidative stress, NF-κB and SIRT1 levels in a STZ-induced experimental diabetes model

ObjectiveThe aim of this study is to investigate the roles of SIRT1 and NF-κB in the pathogenesis of diabetes mellitus in rats with STZ-induced diabetes and determine the effects of hesperidin and quercetin on oxidative stress and on the levels of SIRT1 and NF-κB.Materials and methodsThe experimental animals were divided into four groups, each group comprising ten rats designated as follows: group 1 served as control rats (C); group 2 served as diabetic rats (DM); group 3 served as diabetic rats administered hesperidin (DM + HSP) (100 mg/kg b.w.) in aqueous suspension orally for 15 days; and group 4 served as diabetic rats administered quercetin (DM + Q) (100 mg/kg b.w.) in aqueous suspension orally for 15 days.ResultsIn diabetic group, liver and kidney SIRT1, SOD and CAT activities were significantly lower than control group (p < 0.05). Hesperidin and quercetin caused significant increase in the SIRT1, SOD and CAT activities of both DM + HP and DM + Q groups kidney tissues compared to DM group (p < 0.05). Liver SOD activies were not found to differ significantly between DM, DM + Q and DM + HP groups (p > 0.05). In DM + HP group, liver CAT activities were significantly higher than DM (p < 0.05), but there was no significant difference in liver CAT activities between DM and DM + Q (p > 0.05). In diabetic group, liver and kidney NF-κB and MDA levels were increased compared to control group (p < 0.05), and groups of DM + HP and DM + Q had lower NF-κB and MDA levels than diabetic group (p < 0.05).ConclusionAs a conclusion, based on the results we obtained from this study and the literature data discussed above, we determined in STZ-induced diabetic rats that, increased glucose levels and liver and kidney damage markers decreased significantly after administration of hesperedin and quercetin, and that oxidative stress and NF-κB levels increased while SIRT1 levels decreased in the diabetic group.