Hyperglycemia and advanced glucose end substance (AGE) are responsible for excessive reactive oxygen species (ROS) production, which causes oxidative stress in diabetes mellitus. Oxidative stress and high blood pressure may cause injury and glomerulosclerosis in the kidney. End-stage kidney failure induced by glomerulosclerosis leads to microalbuminuria (Ma) in diabetic nephropathy. We investigated the effects of an angiotensin converting enzyme inhibitor (ACEI), perindopril, and an antioxidant, catechin, on podocytes and the glomerular mesangial matrix in experimental diabetic nephropathy using ultrastructural visualization and immunohistochemical staining.
We compared 5 groups of male adult Wistar albino rats: a control group, an untreated diabetic group, and diabetic groups treated with perindopril, catechin, or catechin+perindopril.
Blood glucose values in all diabetic groups were significantly higher than in the control group (p<0.001). The body weight in all diabetic groups was significantly lower than in the control group (p<0.001, p<0.05). The kidney weight in the catechin+perindopril-treated diabetic group was significantly lower than in the untreated diabetic group (p<0.001). In all treated diabetic groups, Ma levels decreased significantly (p<0.001). Mesangial matrix and podocyte damage increased in the untreated diabetic group, but the group treated with catechin+perindopril showed less damage. TGF-beta 1 immunostaining was significantly lower in the catechin-treated and perindopril-treated groups than in the untreated diabetic group (p<0.001). Catechin was more effective than ACEI in preventing podocyte structure. Podocytes appeared to be the first cells affected in diabetes mellitus. When exposed to hyperglycemia, podocytes caused the mesangial matrix to expand.
Catechin and perindopril were more effective in preventing renal corpuscle damage when administered together.