Silymarin attenuates hepatic and pancreatic redox imbalance independent of glycemic regulation in the alloxan-induced diabetic rat model.

Abstract

Objective To evaluate the efficiency of silymarin (SMN) in modulating metabolic parameters and redox status in rats with type 1 diabetes mellitus (T1DM). Methods Diabetes was induced by intraperitoneal injection of alloxan. The diabetic rats were administered with SMN at doses of 50 and 100 mg/kg body weight/d for 30 consecutive days. The rats were divided into the following four groups: vehicle control, diabetic (alloxan-treated), DS50 (alloxan + 50 mg/kg body weight/d of SMN), and DS100 (alloxan + 100 mg/kg body weight/d of SMN) groups. The bodyweight and food and water intake were evaluated. After 30 d, the animals were euthanized and the blood was collected for measuring the serum levels of glucose, triacylglycerol (TAG), urea, and creatinine. The liver and pancreas were collected for measuring the activities of superoxide dismutase (SOD) and catalase (CAT), and the levels of carbonylated protein (PC). The pancreas sample was also used for histological analysis. Results SMN reduced hepatic (P < 0.001) and pancreatic (P < 0.001) protein damage and creatinine levels (P = 0.0141) in addition to decreasing food (P < 0.001) and water intake (P < 0.001). However, treatment with SMN did not improve beta-cell function or decrease blood glucose levels in diabetic rats. Conclusion SMN improved polyphagia and polydipsia, renal function, and protected the liver and pancreas against protein damage without affecting hyperglycemia in diabetic animals.