{"title":"The role of misoprostol in the prevention of amikacin-induced neuronal damage","authors":"Sebile Azırak , İlkay Armağan","doi":"10.1016/j.tice.2025.102981","DOIUrl":null,"url":null,"abstract":"<div><div>Amikacin (AK) is an aminoglycoside widely used in the treatment of Gram-negative infections which are life-threatening. In the etiology of toxicity, AK has been shown to cause tissue damage through oxidative stress and apoptosis as a consequence of the reactive oxygen species (ROS) production. Misoprostol (MP) is a prostaglangin E1 (PGE1) analogue with antioxidant, antiapoptotic, cytoprotective properties used to prevent gastrointestinal disorders induced by nonsteroidal anti-inflammatory drug. This study aims to investigate the neuroprotective effects of MP on brain cells against the neurotoxicity of AK by gene expression and histopathological analyses. Twenty-four male Spraque-Dawley rats were randomly separated into four groups (group 1, control; group 2, AK; group 3, MP; group 4, AK + MP). According to our findings, AK treatment significantly increased brain weight, brain weight/body weight ratios, and CYP2B1 mRNA gene expression. This was accompanied by histopathological changes such as eosinophilic neurons, pyknotic nuclei, vacuolated neuropil, congestion and inflammation in blood vessels. On the other hand, while significant improvements were observed in brain weight and brain weight/body weight ratios in the AK + MP group, there was a significant decrease in CYP2B1 mRNA gene expression levels and histopathological changes. According to our results, MP may serve as a potential therapeutic candidate to reduce the severity of oxidative damage induced by AK in brain tissue.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 102981"},"PeriodicalIF":2.7000,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tissue & cell","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0040816625002617","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ANATOMY & MORPHOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Amikacin (AK) is an aminoglycoside widely used in the treatment of Gram-negative infections which are life-threatening. In the etiology of toxicity, AK has been shown to cause tissue damage through oxidative stress and apoptosis as a consequence of the reactive oxygen species (ROS) production. Misoprostol (MP) is a prostaglangin E1 (PGE1) analogue with antioxidant, antiapoptotic, cytoprotective properties used to prevent gastrointestinal disorders induced by nonsteroidal anti-inflammatory drug. This study aims to investigate the neuroprotective effects of MP on brain cells against the neurotoxicity of AK by gene expression and histopathological analyses. Twenty-four male Spraque-Dawley rats were randomly separated into four groups (group 1, control; group 2, AK; group 3, MP; group 4, AK + MP). According to our findings, AK treatment significantly increased brain weight, brain weight/body weight ratios, and CYP2B1 mRNA gene expression. This was accompanied by histopathological changes such as eosinophilic neurons, pyknotic nuclei, vacuolated neuropil, congestion and inflammation in blood vessels. On the other hand, while significant improvements were observed in brain weight and brain weight/body weight ratios in the AK + MP group, there was a significant decrease in CYP2B1 mRNA gene expression levels and histopathological changes. According to our results, MP may serve as a potential therapeutic candidate to reduce the severity of oxidative damage induced by AK in brain tissue.
期刊介绍:
Tissue and Cell is devoted to original research on the organization of cells, subcellular and extracellular components at all levels, including the grouping and interrelations of cells in tissues and organs. The journal encourages submission of ultrastructural studies that provide novel insights into structure, function and physiology of cells and tissues, in health and disease. Bioengineering and stem cells studies focused on the description of morphological and/or histological data are also welcomed.
Studies investigating the effect of compounds and/or substances on structure of cells and tissues are generally outside the scope of this journal. For consideration, studies should contain a clear rationale on the use of (a) given substance(s), have a compelling morphological and structural focus and present novel incremental findings from previous literature.