The Protective Effects Of Dihydromyricetin On Kidney Damage In Impaired Glucose Tolerance Rats

Objective:To observe the protective effects of dihydromyricetin on the kidney damage in impaired glucose tolerance rats, and to explore its mechanism from the view of oxidation and the non-enzymatic glycation. To Provide scientific experimental basis on the process of developing dihydromyricetin into diabetes drug or health food.Methods:To produce impaired glucose tolerance animal model, D-galactose was given intraperitoneal injection by increasing progressively dose. Dihydromyricetin was used for subject, metformin for a positive control, fasting blood glucose,postprandial blood glucose in two hours and insulin levels,resistance index; blood and kidney GSH-Px and SOD antioxidant enzymes,MDA,glycosylated hemoglobin,AGEs; blood urea nitrogen and urine microalbumin,cell DNA trailing rate,kidney lactate dehydrogenase as indicatrix, for 8w continuous experiment. To observe dihydromyricetin's impact on oxidative stress and non-enzymatic glycation which were causd by impaired glucose tolerance and to observe it's protective effect on the early damage of kidney.Results:Compared with the normal group, model group's postprandial blood glucose, serum insulin level and insulin resistance index increased significantly(P<0.05); the activity of GSH-Px in serum decreased significantly(P<0.05), the content of MDA and the level of AGEs in serum increased significantly(P<0.05); the activity of SOD in kidney was significantly decreased(P<0.05), the content of MDA in kidney and the level of urinary albumin increased significantly(P<0.05), meanwhile, the renal cell DNA trailing rate and the activity of lactate dehydrogenase significantly increased(P<0.05). Compared with model group, dihydromyricetin group's postprandial blood glucose, serum insulin level and insulin resistance index decreased significantly(P<0.05); the activity of GSH-Px in serum and SOD in kidney improved significantly(P<0.05); the content of MDA in serum and kidney decrease significantly(P<0.05), the level of AGEs in serum and the content of urine microalbumin decrease significantly(P<0.05); the DNA trailing rate and the activity of LDH reduced significantly(P<0.05). Compared with metformin group, there was no significant difference in the other indicatrixes(P>0.05), except the activity of serum GSH-Px in the low dose's dihydromyricetin group which was significant decreased(P<0.05).Conclusion:D-galactose-induced animal model of impaired glucose tolerance, exists oxidative stress,non-enzymatic glycation reaction and early kidney damage. Dihydromyricetin can significantly improve the state of impaired glucose tolerance in rats, have a protective effect in early kidney damage, and its mechanism may related to reducing insulin resistance index, improving the peripheral tissue glucose utilization and having the ability of antioxidant and inhibition of non-enzymatic glycation.