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Abstract
Diabetic neuropathy (DN) commonly occurs in diabetics, affecting approximately 50% of both type 1 and 2 diabetic patients. It is a leading cause of non-traumatic amputations. Oxidative stress could play a key role in the pathophysiology of DN. This study aimed to investigate the potential neuroprotective effect of carvedilol on STZ-induced DN in rats. Thirty male Sprague Dawley rats (weighing 200–250 g) were randomly divided into five groups (six/group), where group 1 (negative control) received only the vehicle (0.5% of carboxymethyl cellulose orally 1 ml/kg). DN was induced by a single injection of remaining rats with streptozotocin (STZ; 50 mg/kg, i.p.). After diabetes induction, group 2 served as the diabetic untreated animals; while groups 3 and 4 were treated with carvedilol (1 and 10 mg/kg/d, orally, respectively). Group 5 received a-lipoic acid as a reference neuroprotective (100 mg/kg/d, orally). All treatments were continued for 45 days after diabetes induction, followed by behavioural tests. After sacrificing the animals, dorsal root ganglia, and sciatic nerves were collected for histopathological examination and biochemical assessments. Briefly, STZ administration caused cold allodynia, induced oxidative stress, and increased nerve growth factor (NGF) concentration. Nevertheless, carvedilol improved the behavioural tests, ameliorated the oxidative imbalance as manifested by reducing malondialdehyde, restoring glutathione content, and superoxide dismutase activity. Carvedilol also decreased NGF concentration in DRG homogenate. In conclusion, this study demonstrates the neuroprotective effect of carvedilol in an experimentally induced DN rat model through–at least partly–its antioxidant effect and reduced NGF concentration in DRG.
Highlights
Diabetes mellitus (DM) is an endocrine disorder that is characterized by hyperglycemia in response to absent or inadequate insulin secretion or impairment of insulin action (Katzung, 2014)
The FBG levels of all treatment groups were significantly elevated compared with the corresponding control at each week
Carvedilol has been revealed by Magadmi et al (Magadmi et al, 2021) to display a neuroprotective effect in vitro in high glucose-induced neuronal damage on cultured dorsal root ganglia
Summary
Diabetes mellitus (DM) is an endocrine disorder that is characterized by hyperglycemia in response to absent or inadequate insulin secretion or impairment of insulin action (Katzung, 2014) It is a major health problem worldwide (Tabish, 2007), with a prevalence of 382 million people and nearly 5.1 million deaths in 2013 (International Diabetes Federation, 2013). In Saudi Arabia, diabetes is prevalent in 24% of its population (International Diabetes Federation, 2013), placing it among the top 10 countries with the highest prevalence rate worldwide (Alzahrani et al, 2015) The impact of both hyperglycemia and vascular impairment results in neuronal dysfunction in the peripheral nervous system (Rahimi-Madiseh et al, 2016). DN is a common occurrence, which affects nearly 50% of patients with diabetes (Tesfaye, 2011)
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