Inhibition Of Nonenzymatic Glycation In Renal Tissue Of Diabetic Rats By TSK

Objective: To investigate into the inhibition and mechanism of TSK on nonenzymatic glycation in renal tissue of diabetic rats. Methods: The rats were randomly divided into 4 groups: normal control group(NC group, n=10), Diabetic group(DM group, n=8) , benazepril treated diabetic group(DTl group, n=9), TSK treated diabetic group(DT2 group, u=10). Body weight, Kidney weight and kidney weight / body weight , as well as blood glucose, serum insulin, 24 hours urinary protein excretion, Creatinine clearance were observed after 4 week of study. The content of AGE in renal tissue were measure respectively. Furthermore, TGF-β1 and TIMP-2 in renal glomerulus were determined with immunohistochemistry. Results: After 4 week treatment, TSK and benazepril could decrease creatinine clearance and 24 hours urinary protein level, as well as suppress kidney hyertrophy in diabetic rats, AGE accmulation in renal tissue were inhibited significantly group in DTI and group in DT2 . Immunohisochemistry analysis showed that overexpress of TOF-β1 and TIMP-2 in renal glomerulus were down-regulated by TSK and benazepril. Moveover, TSK could ameliorate hyperglycemia, and increase serum insulin level. Conclusion: TSK may inhibit nonezymatic glycation of protein and AGE formation in renal tissue, which may be one of the important mechanisms of its nephroprotection.