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Abstract
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Diabetes mellitus (DM) refers to a chronic metabolic disorder that is characterized by a persistent hyperglycemia resulting from defects in insulin secretion, insulin action, or both [1]. Diabetes is increasing all over the world and represents an important public health problem. Hyperglycemia has long-term consequences that cause damage and dysfunction of many organs, particularly the eyes, kidneys, nerves, heart, and blood vessels [1, 2]. One of the crucial underlying mechanisms behind diabetes complications is oxidative stress, which happens when the generation of reactive oxygen species (ROS) outpaces the capacity of the body's antioxidant defense system [2].
Oxidative stress plays an important role in the pathogenesis of beta-cell dysfunction, insulin resistance, and diabetes complications. Malondialdehyde (MDA) is a lipid peroxidation product widely used as a biomarker of oxidative damage to cell membranes, while superoxide dismutase (SOD) is an essential antioxidant enzyme responsible for the degradation of superoxide radicals and protection against oxidative injury [3]. Dysregulation of these biomarkers is a specific feature of diabetes-induced oxidative stress and hence informative markers in experimental studies.
Melittin, the main active component of honey bee venom, is an amphipathic cationic peptide with a wide range of multifunctional biological activities including anti-inflammatory, antioxidant, and cytoprotective activities [4, 5]. Earlier studies have shown that melittin regulates intracellular ROS levels, inhibits apoptosis, and elevates antioxidant defense systems in various cell and animal models [4, 6]. In spite of such observations, few reports are found on the direct effect of melittin on oxidative stress biomarkers like MDA and SOD in streptozotocin-induced diabetic rats, a very popular experimental model of type 1 diabetes.
The current research, therefore, aims to fulfill this requirement by determining the effect of the administration of m
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