Ayvaz S.Aksu B.Karaca T.Cemek M.Tarladacalisir Y.-T.Ayaz A.Metin M.-S.2024-06-122024-06-1220141108-4189https://hdl.handle.net/20.500.14551/17261Background: We studied whether methylene blue (MB) treatment blunts chest trauma-induced lung injury in rats. Material and Methods: Forty male Sprague-Dawley rats, 200-300g, were used. The rats were divided into five groups (n=8): control, early contusion (EC), early contusion + methylene blue (2 mg/kg, EC+MB), late contusion (LC), and late contusion + methylene blue (2 mg/kg, LC+MB). Results: Histopathological analysis showed increased hemorrhage, alveolar wall thickness, edema, and inflammatory cell infiltrates in the EC and LC rats, which decreased upon MB treatment. Immunohistochemical studies revealed that MB reduced activation of inducible nitric oxide synthase (iNOS) and the number of active terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells. A significant increase was observed in the malondialdehyde (MDA) and nitric oxide (NO) levels in the EC group compared to the control group (p<0.05). In addition, a significant decrease was reported in the glutathione (GSH), superoxide dismutase (SOD), and glutathione peroxidase (GPx) levels (p<0.01), but no significant difference was observed in the catalase (CAT) levels among the groups. The MDA level was significantly higher in the LC group compared to the control group, whereas the GSH level was significantly lower compared to the control group. The NO level in the EC+MB group was significantly lower when compared to the NO level in the EC group (p<0.05). Conclusion: The present study provides evidence that MB might serve as a therapeutic treatment for blunt chest trauma.eninfo:eu-repo/semantics/closedAccessAntioxidants; Blunt Chest Trauma; Contusion; Methylene Blue; OxidantsCatalase; Glutathione; Glutathione Peroxidase; Inducible Nitric Oxide Synthase; Malonaldehyde; Methylene Blue; Nitric Oxide; Superoxide Dismutase; Acute Lung Injury; Alveolar Wall Thickness; Animal Cell; Animal Experiment; Animal Model; Animal Tissue; Article; Controlled Study; Drug Effect; Enzyme Activation; Histopathology; Immunohistochemistry; Inflammatory Infiltrate; Lung Contusion; Lung Edema; Lung Hemorrhage; Male; Nick End Labeling; Nonhuman; Oxidative Stress; Rat; Respiratory Tract Parameters; Thorax Blunt TraumaArticle18150562-s2.0-84899419169Q4