Abstract
Background: Although ethanol exerts its neurotoxic effect on the brain through inflammatory and oxidative processes, the effect of Riboceine on the brain following ethanol neurotoxicity is yet to be elucidated. Therefore, this study was designed to evaluate the effects of riboceine on the cellular, behavioral, and molecular impairments induced by ethanol toxicity in rats. Methods: A total of 24 male Wistar rats weighing between 160-170 grams were used for the study, and were divided into four groups of six rats each. After completion of the administration of ethanol and riboceine, and testing for motor impairment, the rats were sacrificed. The cerebellum was excised and processed for oxidative stress analyses, based on oxidative stress markers and histological examinations. The immunohistochemical expression of astrocytes in the cerebellum was examined, using Glial Fibrillary Acidic Protein (GFAP) stain. Results: This study demonstrated that ethanol-induced neurotoxicity in the cerebellum, characterized by increased oxidative stress profile, astrocyte activation, and neuronal death in the cerebellum, especially the Purkinje layer. Necrosis, significant decrease in Superoxide Dismutase (SOD), Catalase (CAT) and Gluathione (GSH) activities (P<0.05) as well as astrogliosis was associated with ethanol treatment. However, riboceine was observed to significantly increase the cerebellar SOD, CAT and GSH activities with significantly reduced Malondialdehyde (MDA) levels (P<0.05). It also attenuated the histomorphological alteration of the cerebellum and reduced the cerebellar astrocytes activation following ethanol-induced neurotoxicity, thus leading to the attenuation of motor impairment. Conclusion: Riboceine attenuated motor impairment caused by chronic ethanol-induced neurotoxicity, suggestive of its anti-oxidative and anti-inflammatory properties.
Highlights
E thanol is a psychoactive substance that is widely used after caffeine [1]
Significant decrease in Superoxide Dismutase (SOD), Catalase (CAT) and Gluathione (GSH) activities (P
Though the mechanism by which riboceine inhibits the up-regulation of Glial Fibrillary Acidic Protein (GFAP) is not fully understood, our findings suggest that the anti-inflammatory property of riboceine may play a significant role in this inhibitory process of astrocyte activation in the cerebellar cortex secondary to the ethanol neurotoxicity
Summary
Chronic alcohol use presents a major public health hazard that is associated with various diseases and toxicities, especially among young people. The liver breaks down the majority of ingested ethanol, it has deleterious effects on the brain and other organs [2]. Ethanol is known to disrupt the oxidative balance, through a process termed neuroexcitotoxicity, which leads to the development of oxidative stress. Ethanol-induced oxidative stress leads to various medical disorders, such as hepatic, cardiovascular, and other alcohol-induced neurotoxic damages [3]. Ethanol exerts its neurotoxic effect on the brain through inflammatory and oxidative processes, the effect of Riboceine on the brain following ethanol neurotoxicity is yet to be elucidated. This study was designed to evaluate the effects of riboceine on the cellular, behavioral, and molecular impairments induced by ethanol toxicity in rats
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