DMP-1 attenuates oxidative stress and inhibits TGF-β activation in rats with diabetic kidney disease.

Introduction: DMP-1 supplement has a satisfactory effect on diabetic kidney disease in patients with whether T1DM or T2DM. Oxidative stress and TGF-beta signal pathway activation are essential in the pathogenesis of DKD. We aim to investigate the effect of DMP-1 on oxidative stress and TGF-beta activation in rats with DKD. Materials and methods: Male Wistar rats were enrolled and randomly allocated into five groups: Control group, STZ group (60 mg/kg, ip), DMP-1 low dose group (0.5 g/kg/day, ig), DMP-1 medium dose group (1.0 g/kg/day, ig) and DMP-1 high dose group (2.0 g/kg/day, ig). The levels of UREA, BUN, UCr, beta(2)-MG, mALB, NOS, CAT, MDA and T-AOC were measured after 8 weeks treatment. And rats' left kidneys were harvested to detect the expression of TGF-beta, Smad2/3 and Smad7 by immunohistochemical analysis. Results: DMP-1 treatment has protective effects on kidney injury induced by STZ, which is demonstrated as following criteria: (1) a significant reduction in levels of UREA (p<0.05), BUN (p<0.05), UCr (p<0.05), b2-MG (p<0.05) and mALB (p<0.05) in rats treated by DMP-1 compared with the ones injected with STZ only; (2) an apparent increment levels of NOS (p<0.05), CAT (p<0.05) and T-AOC (p<0.05), while reduction in level of MDA (p<0.05) in DMP-1 groups compared with STZ group; (3) a significant inhibition of TGF-beta and Smad2/3 overexpression induced by STZ in kidney tissue. What's more, DMP-1 can increase Smad7 expression. Conclusion: DMP-1 could slow pathological process and protect kidney from DKD injury by decreasing oxidative stress and inhibiting TGF-beta signal pathway activation in rats.