The Neuroprotective Effect of Carvedilol on Diabetic Neuropathy: An In Vitro Study

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.

Figure 1

Effect of high glucose medium (45 mM) on DRG culture viability at different time points.

Figure 2

Procedure followed in this in vitro study.

Figure 3

Calcein-AM-stained fluorescent image of the DRG culture.

Figure 4

Carvedilol effect on HG-induced decreases in DRG viability.

Figure 5

Effect of the carvedilol on neurite length in high-glucose media.

Figure 6

Effect of the carvedilol on soma perimeter in high-glucose media.

Figure 7

Effect of the carvedilol on soma area in high-glucose media.

Figure 8

Percentage of ATF-positive neurons in high-glucose DRG cultures.