Adeshina O Adekeye, Adedamola A Fafure, Darell E Asira, Ayoola E Ogunsemowo
{"title":"Anti-oxidative and anti-inflammatory role of naringin against vanadium-induced neurotoxicity in adult Wistar rats","authors":"Adeshina O Adekeye, Adedamola A Fafure, Darell E Asira, Ayoola E Ogunsemowo","doi":"10.52083/eunf6102","DOIUrl":null,"url":null,"abstract":"Vanadium is a trace element that can induce oxidative damage in the brain due to excess accumulation, which leads to programmed neuronal cell death. Naringin as a natural flavonoid has been reported to have a broad range of pharmaceutical bioactivities. We aimed to explore the therapeutic effects of naringin against oxidative stress and inflammation induced by vanadium exposure. Forty adults male Wistar rats were indiscriminately distributed into four (4) groups (n = 10). The groups received the followinh treatments: 5 ml/kg double distilled water (control), Naringin (Intraperitoneally, 30mg/kg BW), Vanadium & Naringin (Vanadium at 10mg/kg & Naringin at 30mg/kg respectively), Vanadium (Intraperitoneally, 10mg/ kg BW). The result of vanadium administration showed an increase in oxidative stress, as seen in the reduction of glutathione peroxidase and catalase level of the brain (hippocampus), a decrease in numbers of viable cells and significant increase in inflamed cells. A decrease in memory function following vanadium administration was also observed. Therapeutic administration with naringin following vanadium exposure showed an elevation of glutathione peroxidase levels and catalase level of the hippocampus, a significant decrease in the number of inflamed cell and an improvement in memory function. This study is a proof that naringin can serve as a neuroprotective agent against oxidative stress and inflammation following vanadium toxicity in the brain.","PeriodicalId":11978,"journal":{"name":"European journal of anatomy","volume":"26 1","pages":""},"PeriodicalIF":0.3000,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"European journal of anatomy","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.52083/eunf6102","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"ANATOMY & MORPHOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Vanadium is a trace element that can induce oxidative damage in the brain due to excess accumulation, which leads to programmed neuronal cell death. Naringin as a natural flavonoid has been reported to have a broad range of pharmaceutical bioactivities. We aimed to explore the therapeutic effects of naringin against oxidative stress and inflammation induced by vanadium exposure. Forty adults male Wistar rats were indiscriminately distributed into four (4) groups (n = 10). The groups received the followinh treatments: 5 ml/kg double distilled water (control), Naringin (Intraperitoneally, 30mg/kg BW), Vanadium & Naringin (Vanadium at 10mg/kg & Naringin at 30mg/kg respectively), Vanadium (Intraperitoneally, 10mg/ kg BW). The result of vanadium administration showed an increase in oxidative stress, as seen in the reduction of glutathione peroxidase and catalase level of the brain (hippocampus), a decrease in numbers of viable cells and significant increase in inflamed cells. A decrease in memory function following vanadium administration was also observed. Therapeutic administration with naringin following vanadium exposure showed an elevation of glutathione peroxidase levels and catalase level of the hippocampus, a significant decrease in the number of inflamed cell and an improvement in memory function. This study is a proof that naringin can serve as a neuroprotective agent against oxidative stress and inflammation following vanadium toxicity in the brain.
期刊介绍:
El European Journal of Anatomy es continuación de la revista “Anales de Anatomía”, publicada en español desde 1952 a 1993. Tras unos años de interrupción debido fundamentalmente a problemas económicos para su mantenimiento, la Sociedad Anatómica Española quiso dar un nuevo impulso a dicha publicación, por lo que fue sustituido su título por el actual, además de ser publicada íntegramente en inglés para procurar así una mayor difusión fuera de nuestras fronteras. Este nuevo periodo se inició en 1996 completándose el primer volumen durante el año 1997.