Antidiabetic effect of olive leaf extract on streptozotocin-induced diabetes mellitus in experimental animals.

Abstract

Background: recently, a relationship between diabetic complications and oxidative stress has been emphasized. There have been some studies showing the effect of olive leaf on hyperglycemia and diabetic complications due to its antioxidant properties. In many studies the effect of olive leaf on plasma total antioxidant level has been measured by different methods. Our study represents the first time it has been measured by a new method of total thiol disulfide homeostasis. Aim: chronic exposure to hyperglycemia and hyperlipidemia contributes to the pathogenesis of diabetic complications through oxidative stress mediators. Thiol is one of the most important antioxidant barriers in humans, and thiol disulfide homeostasis is a new oxidative stress marker. We aimed to investigate the effect of olive leaf extract (OLE) obtained from fresh leaves of Olea europaea, var oleaster on diabetic complications through their hypoglycemic and antioxidant effect in diabetic rats. Methods: twenty-eight Wistar albino rats aged 12-13 weeks were used in the study. The rats were divided into a control group (C), a diabetic control group (DC), a diabetic group treated with 200 mg/kg OLE (D+200), and a diabetic group treated with 400 mg/kg OLE (D+400), having 7 rats in each group. The treatment groups received OLE by the gavage method for 21 days. At the end of the study, all rats were sacrificed by cervical dislocation. Blood samples collected from the heart were centrifuged and glucose, total cholesterol, triglyceride, urea, uric acid, creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), lipid hydroperoxide (LOOH) level, and thiol-disulfide homeostasis were determined. The hemoglobin A1c (HbA1c) analysis was performed on complete blood. In addition, a tail flick test and hot plate modeling were performed to indicate pain perception loss. Results: it was observed that OLE had no effect on serum glucose and HbA1c levels. On the contrary, OLE reduced the levels of total cholesterol (p < 0.01), urea (p < 0.01) and hot plate latency (p < 0.01) in a significant manner. Also, OLE showed a tendency to reduce LOOH levels and to increase thiol levels in a dose-dependent manner (p > 0.05). Conclusion: OLE supplementation for 21 days, at the amounts used, cannot protect against hyperglycemia but may be protective against hypercholesterolemia and tissue damage as caused by diabetes mellitus in rats.