The protective effect of Satureja bachtiarica hydroalcoholic extract on streptozotocin‐induced diabetes through modulating glucose transporter 2 and 4 expression and inhibiting oxidative stress

Abstract

Context: Oxidative stress plays an important role in development of diabetes mellitus. Satureja bachtiarica Bunge (Lamiaceae) is a rich source of bioactive compounds with antioxidant properties.

Objective: This study investigates the antidiabetic effect of hydroalcoholic extract of aerial parts of S. bachtiarica.

Methods and materials: Male Wistar rats were randomly divided into six groups (n = 8) including control (normal saline), diabetic [Streptozotocin (STZ)], intervention (STZ plus hydroalcoholic extract of S. bachtiarica at doses of 75, 150 and 250 mg/kg/d) and positive control (STZ plus captopril 50 mg/kg/d) groups. A single intraperitoneal (IP) injection of STZ (60 mg/kg) was used to induce diabetes and IP therapy with drugs was performed for four weeks.

Results: In diabetic rats, serum total antioxidant capacity (TAC) decreased significantly, but glucose, alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutamyltransferase (GGT) and malondialdehyde (MDA) increased significantly as compared to the control (p < 0.05). Treatment with extract (250 mg/kg) caused a significant decline in serum glucose, GGT, ALT, AST and MDA as well as a significant increase in serum TAC (p < 0.05). During the intervention period, diabetic rats showed significant weight loss, but extract (250 mg/kg) treated rats did not show any weight loss. Extract (250 mg/kg) up-regulated GLUT2 expression and down-regulated GLUT4 expression in the liver (p < 0.05). S. bachtiarica extract at all dosage levels prevented STZ-induced histological damage of liver, kidney and pancreas.

Discussion and conclusions: S. bachtiarica extract exhibits antidiabetic effects through modulation of oxidative stress and expression of GLUT2 and GLUT4.

Keywords:

• Satureja bachtiarica
• diabetes
• streptozotocine
• oxidative stress
• glucose transporter

Acknowledgements

The authors would like to thank the staff of laboratory of Islamic Azad University Izeh, Iran for assisting in conducting this work. This article has been derived from the MSc thesis.

Disclosure statement

No potential conflict of interest was reported by the authors.