| Advanced glycation end products(AGEs)are a heterogeneous group of compounds that are formed by non-enzymatic reactions between reducing sugars and the free amino groups of proteins,lipids or nucleic acids.In recent years,the relationship between diet-derived AGEs and kidney damage has been received much attention.Although many studies have demonstrated that dietary AGEs intake have an impact on the kidney,it is mainly targeted at short-term studies.However,the mechanism of long-term high AGEs diet on the structure and function of the kidney in healthy individuals has not yet been fully elucidated.In this study,C57BL/6 male mice were used as animal model.The effect of long-term intake of dietary AGEs on kidney of mice was studied by diet with different AGEs for 12 months.The following main conclusions are drawn:(1)Dietary AGEs intake had no significant effect on lipid metabolism in mice(P>0.05).The serum BUN levels,creatinine levels and albumin excretion rate significantly increased after 12 months of high AGEs diet(P<0.05).(2)With the extension of feeding time,the kidney CML content of mice showed a gradual increase trend.The accumulation of CML in renal cortices at 12 momths of feeding were significantly increased in the H-AGEs group than in the N-AGEs group(P<0.05).After12 months of high AGEs diet,the activities of total-superoxide dismutase(T-SOD)activity and glutathione peroxidase(GSH-PX)activity in kidney were significantly decreased(P<0.05).The content of malonaldehyde(MDA)in the H-AGEs group were higher than those in the N-AGEs group,but there was no significant difference(P>0.05).(3)High AGEs diet upregulates the receptor for advanced glycation end products(RAGE)levels in the kidney.At 6,8,10 and 12 months of feeding,there was a significant difference in RAGE levels between the two groups(P<0.05);At 12 months of feeding,the activities of interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)in kidney of mice were significantly increased(P<0.05);Histological examination of renal tissue showed progressive histopathological changes in kidney. |