Abstract

SUMMARY
Aim/Backgrounds
Ischemia-reperfusion injury (IRI) results in oxidative stress. The present research investigates the ozone administration in rats IRI through histopathological and biochemical assessments.
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, it was found 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

Key words: Keywords: ischemia–reperfusion injury, ozone therapy, skeletal muscle, oxidative stress, rat