Abstract:

Objective    To study the effect of oral advanced glycation end products(AGEs) on rats with diabetic nephropathy(DN) and its mechanism. Methods    10 rats were randomly selected from 40 male Sprague-Dawley rats as the control group. The other 30 rats which  developed DN were randomly divided into three groups: the AGEs-rich diet group, the AGEs-poor diet group and the common diet group, 10 rats in each group. Each group was studied at the 9th and 13th weeks. The following parameters were detected with different methods: 24 h urinary albumin with the Coomassie brilliant blue method, serum creatinine and urine creatinine by an automatic biochemistry analyzer, content of MDA in 24 h urine and nephridial tissue homogenate by TBARS, content of CML in serum and nephridial tissue homogenate by ELISA, and activity of SeGSHPx in serum and nephridial tissue homogenate by a spectrophotometer. Ccr was calculated.  Results     Significant differences were found between the three DN  groups and the control group（P＜0.05）. Compared to the common diet group, the following variables in the AGEs-rich diet group were dramatically increased: the 24 h urine protein, MDA levels in 24 h urine and nephridial tissue homogenate, and CML levels in serum and nephridial tissue homogenate（P＜0.05); while SeGSHPx activities in serum and nephridial tissue homogenate decreased（P＜0.05). In contrast, the AGEs-poor diet group showed opposite results in all the above variables. No significant difference was observed in Scr and Ccr among the three DN rat groups（P＞0.05）. Conclusion    An AGEs-rich diet impairs the renal function of DN rats and the mechanism is probably related to damage to anti-oxidation ability and enhancement of oxidative stress.

Key words: Advanced glycation end products; Diabetic nephropathy; Oxidative stress; Malondialdehyde; Se-glutathione peroxidase