Background and Aim: Diabetes Mellitus (DM) is associated with increased oxidative stress and its related complications. The phenolic components of mulberry (Morus nigra L.) leave have antioxidant components that can modulate oxidative stress. In this study, the beneficial effects of mulberry leaves extract were assessed in diabetic nephropathy and liver cells damage.
Materials and Methods: Diabetes induced by high-fat diet and injection of 35 mg/kgBW Streptozotocin (STZ). Forty-four male wistar rats were divided into four groups: healthy control, non-treated, glibenclamide-treated, and extract-treated. The extract-treated group was treated with mulberry leaf extract for 4 weeks. At the end of treatment, kidney, liver and blood samples were collected to assay the biochemical analysis including fasting blood glucose level, albumin, creatinine, urea and uric acid concentrations, white blood cells, hemoglobin, hematocrit and histological evaluation.
Results: Fasting blood glucose, creatinine, urea and uric acid were significantly in low levels in extract-treated group compared with the non-treated diabetic rats (p<0.001, p=0.03, p=0.009, and p=0.002; respectively). White blood cells level was low level (p<0.001) and hemoglobin and hematocrit levels were higher in extract treated group (p<0.001 and p=0.01; respectively). Serum albumin level in extract-treated rats was significantly higher than untreated group (p<0.001). Evaluating the histopathology of kidney showed that glycogen accumulation, fatty degeneration, and lymphocyte infiltration in extract-treated group were mild; while they were moderate in non-treated group; moreover, liver tissue evaluation showed that the fatty degeneration in extracttreated rats was mild and the cytoplasm of hepatocytes was distended by smaller amount of fatty droplets.
Conclusion: The antioxidant properties of Mulberry leaves inhibited kidney and liver damage in diabetic rats. These results can be a base to evaluate the effects of mulberry (Morus nigra L.) leaves extract in the management of hyperuricemia, nephropathy, and fatty degeneration in liver cells in diabetic human patients.