Abstract
Diabetic neuropathy serves as a major complication for diabetic patients across the world. The use of effective treatment is integral for reducing the health complications for diabetic patients. This study has evaluated the carvedilol potential neuroprotective effect on diabetic neuropathy. An in vitro model of diabetic neuropathy was used, including dorsal root ganglia (DRG) that were cultured from male adult mice C57BL. These were incubated for about twenty-four hours in high glucose (HG) media (45 mM). Some cells were incubated with carvedilol (10 μM). Neuronal viability, neuronal morphology, and activating transcription factor 3 (AFT3) were measured. The cell viability was decreased, along with neuronal length, soma area, and soma perimeter with HG media. Also, there was an overexpression of ATF3, which is a neuronal stress response marker. The pretreatment with carvedilol increased the viability of DRG as compared to HG-treated cells. Also, it significantly protected the DRG from HG-induced morphology changes. Though it shows a decrease in AFT3 expression, the statistical results were insignificant. The current study demonstrates the neuroprotective effect of carvedilol against HG-induced DN using an in vitro model. This could be through carvedilol antioxidant effects.
Highlights
The prevalence of diabetic neuropathy (DN) is recognized to affect about 50 percent of diabetic patients
In order to evaluate the neuroprotective effect of carvedilol in diabetic neuropathy, dorsal root ganglia (DRG) cultures with high glucose (HG) media were incubated with or without carvedilol
The DRGs exposed to HG media showed more than 20% significantly decreased cell viability compared to the corresponding control (p = 0:0001)
Summary
The prevalence of diabetic neuropathy (DN) is recognized to affect about 50 percent of diabetic patients (both type 1 and type 2). Most studies confirm the DN as the major reason for diabetic patient’s hospitalization as well as nontraumatic amputations [1]. Callaghan et al [2] state that the management of DN is generally attained through appropriate blood glucose levels within the normal range and symptomatic therapy. Various researches have explored DN chronic pain management, only a few improvements are achieved, where the remaining fail to meet the clinical needs of DN [3]. Tesfaye [4] noted that only two compounds show a clinical improvement, namely, α-lipoic acid and epalrestat. Tesfaye [4] and Kumar and
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