Akademik Veri Yönetim Sistemi
Turkish Journal of Vascular Surgery, cilt.34, sa.3, ss.220-225, 2025 (Scopus, TRDizin)
Aim: Ischemia-reperfusion injury (IRI) results in oxidative stress. The present research investigates ozone administration in rats IRI through histopathological and biochemical assessments. Material and Methods: We assigned 24 rats, Wistar albino, into four randomized groups (n = 6 each): S, O, IRI and IRI + O. The aorta was clamped for 45 minutes, and reperfusion was followed by 120 minutes to induce IRI. Ozone (0.7 mg/kg, intraperitoneal) was administered before the reperfusion period in the IRI + O and without ischemia in the O. Muscle tissues were evaluated histopathologically in terms of neutrophil infiltration, hemorrhage, interstitial edema, and myocyte damage. In addition, biochemical analyses were performed to measure malondialdehyde (MDA) and glutathione (GSH) levels. Results: Remarkably elevated MDA values were found in the IRI than the S and O. (p=0.007 and 0.006, respectively). Although ozone reduced MDA in the IRI + O, this reduction did not meet statistical significance. GSH values were considerably decreased in the IRI according to the S and O (p=0.010 and p=0.001, respectively); but, they were elevated in the IRI + O than the IRI (p=0.007). Histopathology demonstrated significantly reduced hemorrhage, neutrophil infiltration, muscle injury, and interstitial edema in the IRI + O than the IRI (p<0.001, p=0.037, p=0.042, and p=0.029, respectively). Conclusion: Ozone therapy mitigates IR–induced skeletal muscle injury by reducing histological alterations and enhancing antioxidant defenses in rats. These findings suggest ozone as a potential agent in IRI management; however, further research is required to optimize dosing and timing.