The role of misoprostol in the prevention of amikacin-induced neuronal damage
Tissue and Cell, cilt.96, 2025 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 96
- Basım Tarihi: 2025
- Doi Numarası: 10.1016/j.tice.2025.102981
- Dergi Adı: Tissue and Cell
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, Veterinary Science Database
- Anahtar Kelimeler: Amikacin, Apoptosis, Brain, CYP2B1, Misoprostol
- Süleyman Demirel Üniversitesi Adresli: Evet
Özet
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.