Title of article :
Diosgenin attenuates cardiac oxidative stress in streptozotocin- induced diabetic rat
Author/Authors :
Golshahi، Jafar نويسنده Associate Professor, Isfahan Cardiovascular , , Roghani-Dehkordi، Farshad نويسنده Department of Cardiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran ,
Issue Information :
دوفصلنامه با شماره پیاپی 0 سال 2016
Pages :
6
From page :
13
To page :
18
Abstract :
Background and Objective: Chronic diabetes mellitus (DM) leads to cardiovascular dysfunction. Diosgenin is a natural steroidal saponin with cardiovascular protective potential. In this research study, the beneficial effect of diosgenin was evaluated on some markers of oxidative stress in cardia tissue of streptozotocin (STZ)-diabetic rats. Materials and Methods: Male Wistar rats (n = 28) were divided into equal-sized control, diosgenin-treated control, diabetic, and diosgenin-treated diabetic groups. Diabetes was induced by a single intraperitoneal injection of streptozotocin (60 mg/kg). Diosgenin was administered p.o. at a dose of 40 mg/kg for 7 weeks. Some markers of oxidative stress including malondialdehyde (MDA), superoxide dismutase (SOD), catalase, and reduced glutathione (GSH) were measured in cardiac tissue homogenate. Results: It was found out that diabetic group had an elevated MDA content (p < 0.01), reduced activity of SOD (p < 0.05) and catalase (p < 0.05) and a lower content of GSH (p < 0.01) versus control group and chronic diosgenin treatment significantly reversed only MDA (p < 0.05) and GSH (p < 0.05) with no significant effect on SOD activity and catalase activity. Conclusion: Diosgenin could attenuate cardiac lipid peroxidation and improves non-enzymatic antioxidant defensive system in diabetic condition and it may be considered as a potential therapeutic agent to mitigate cardiac dysfunction in DM.
Journal title :
Journal of Basic and Clinical Pathophysiology
Serial Year :
2016
Journal title :
Journal of Basic and Clinical Pathophysiology
Record number :
2385913
Link To Document :
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