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1- Department of Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, Osun State University, Osogbo, Osun State, Nigeria.
2- Department of Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, Osun State University, Osogbo, Osun State, Nigeria. , olorunfemi.tokunbo@uniosun.edu
3- Department of Radiology, Faculty of Clinical Sciences, Ekiti State University, Ekiti State, Nigeria.
4- Department of Anatomy and Cell Biology, Faculty of Basic Medical Sciences, College of Health Sciences, Obafemi Awolowo University, Ile-ife, Osun State, Nigeria.
Abstract:   (67 Views)
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 SOD, CAT and GSH activities (P<0.05) as well as astrogliosis was associated with ethanol treatment. However, riboceine was observed to significantly increase the cerebellar superoxide dismutase (SOD), catalase (CAT) and glutathione 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.
Conclusions: Riboceine attenuated motor impairment caused by chronic ethanol-induced neurotoxicity, suggestive of its anti-oxidative and anti-inflammatory properties.
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Type of Study: Research | Subject: General

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