Abstract

Diabetic neuropathy (DN) is a widespread disabling disorder including peripheral nerves' damage. The aim of the current study was to estimate the potential ameliorative effect of Dunaliella salina (D. salina) on DN and the involvement of the thioredoxin. Diabetes was induced by streptozotocin (STZ; 50 mg/kg; i.p). Glimepiride (0.5 mg/kg) or D. salina powder (100 or 200 mg/kg) were given orally, after 2 days of STZ injection for 4 weeks. Glucose, total antioxidant capacity (TAC), superoxide dismutase (SOD), and catalase (CAT) serum levels as well as brain contents of thioredoxin (Trx), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) were measured with the histopathological study. STZ-induced DN resulted in a significant (P < 0.05) rise in glucose blood level and brain contents of TNF-α and IL-6 and produced a reduction in serum TAC, SOD, CAT, and brain Trx levels with irregular islets of Langerhans cells and loss of brain Purkinje cells. Treatment with glimepiride or both doses of D. salina alleviated these biochemical and histological parameters as compared to the STZ group. D. salina has a neurotherapeutic effect against DN via its inhibitory effect on inflammatory mediators and oxidative stress molecules with its upregulation of Trx activity.

Highlights

  • Diabetic neuropathy (DN) is the most common diabetes complication and its prevalence ranges from 40% to 50% of patients with diabetes

  • Hyperglycemia is considered a central key to DN pathogenesis and induces the formation of reactive oxygen species (ROS) damaging the nerves [3, 4] and provokes sensory symptoms that start in the toes affect the upper limbs by time which is diagnosed by loss of pain sensation [5] using thermal hot plate test [6]

  • Glucose is necessary to supply central nervous system with energy [7] and hyperglycemia in diabetes can induce a variety of complications such as nephropathy, retinopathy, and increased risk of cardiovascular disease [8] that are induced by an injection of streptozotocin (STZ) that selectively destructs insulin-producing β-cells of the pancreas experimentally and leads to brain injury [9]

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Summary

Introduction

Diabetic neuropathy (DN) is the most common diabetes complication and its prevalence ranges from 40% to 50% of patients with diabetes. Hyperglycemia is considered a central key to DN pathogenesis and induces the formation of reactive oxygen species (ROS) damaging the nerves [3, 4] and provokes sensory symptoms that start in the toes affect the upper limbs by time which is diagnosed by loss of pain sensation [5] using thermal hot plate test [6]. Glucose is necessary to supply central nervous system with energy [7] and hyperglycemia in diabetes can induce a variety of complications such as nephropathy, retinopathy, and increased risk of cardiovascular disease [8] that are induced by an injection of streptozotocin (STZ) that selectively destructs insulin-producing β-cells of the pancreas experimentally and leads to brain injury [9]

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