Selenium downregulates RAGE and NFκB expression in diabetic rats.

Area of Science:

• Biochemistry
• Endocrinology
• Toxicology

Background:

• Diabetes mellitus is a major global health concern, contributing significantly to mortality.
• Oxidative stress is implicated as a key factor in the development of diabetic vascular complications.
• Selenium exhibits insulin-like actions and antioxidant properties, suggesting a potential therapeutic role.

Purpose of the Study:

• To investigate the protective effects of selenium, administered as sodium selenite, on streptozotocin-induced diabetes in rats.
• To evaluate the impact of selenium on key markers of diabetes and oxidative stress.

Main Methods:

• Induction of diabetes in rats using streptozotocin.
• Administration of sodium selenite at a dose of 1 μg/kg body weight.
• Assessment of antioxidant enzyme activities, serum glucose, glycated hemoglobin, and lipid peroxidation.
• Evaluation of NFkB and RAGE gene expression.
• Histopathological examination of tissues.

Main Results:

• Selenium supplementation normalized the activities of antioxidant enzymes that were altered by streptozotocin.
• A significant decrease in serum glucose and glycated hemoglobin levels was observed.
• Lipid peroxidation product levels were reduced, indicating decreased oxidative stress.
• Downregulation of NFkB and RAGE expressions was noted.
• Histopathological findings supported the protective role of selenium.

Conclusions:

• Selenium, as sodium selenite, demonstrates a significant protective effect in streptozotocin-induced diabetes mellitus.
• Selenium mitigates diabetes-related complications by reducing oxidative stress and modulating key inflammatory pathways.
• These findings highlight selenium's potential as a therapeutic agent for managing diabetes.