Abdulkadir AKSOY, Ergul Belge KURUTAS, İlter DEMİRHAN
Journal of Basic and Clinical Health Sciences - 2026;10(1):32-41
Purpose: Cerebral ischemia/reperfusion (I/R) injury poses a serious threat to human health. This study aimed to investigate the effects of commonly used intravenous anesthetics on oxidant and antioxidant status as well as neuron-specific enolase (NSE) levels in an experimental I/R model. Material and Methods: The study animals were divided into the following five groups: group I, sham (did not receive drugs); group II, control (only I/R, but did not receive drugs); group III, (I/R ketamine) (the I/R model was used, and the animals were treated with 20 mg/kg ketamin intraperitoneally 30 minutes after the ischemia); group IV (I/R-thiopental) (the I/R model was used, and the animals were treated with 20 mg/kg thiopental intraperitoneally 30 minutes after the ischemia): group V, (I/R propofol) (the I/R model was used, and the animals were treated with 20 mg/kg propofol intraperitoneally 30 minutes after the ischemia). At the end of the reperfusion phase, brain tissue samples were collected for biochemical and histopathological examinations. Biomarkers of oxidative stress, including catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA), were measured spectrophotometrically. ELISA measured the level of neuron-specific enolase. Histopathological analysis was performed under a light microscope. Results: In the control group, ischemia-reperfusion significantly increased MDA and NSE levels and decreased antioxidant enzyme activities (p < 0.05). In contrast, the ketamine, thiopental, and propofol groups showed significantly lower MDA and NSE levels and higher antioxidant enzyme activities compared with the control group (p < 0.05). Histopathological examination revealed that the ketamine, thiopental, and propofol groups exhibited reduced neuronal damage and evidence of regeneration. Conclusion: This study provides in vivo evidence that certain anesthetic agents exert protective effects against cerebral ischemia-reperfusion injury by modulating oxidative stress and neuronal damage.
