| Autor: |
Özer A; Department of Cardiovascular Surgery, Faculty of Medicine, Gazi University, Ankara 06510, Turkey., Şengel N; Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, Gazi University, Ankara 06490, Turkey., Küçük A; Department of Physiology, Faculty of Medicine, Kutahya Health Sciences University, Kutahya 43020, Turkey., Yığman Z; Department of Histology and Embryology, Faculty of Medicine, Gazi University, Ankara 06510, Turkey.; Neuroscience and Neurotechnology Center of Excellence (NÖROM), Gazi University, Ankara 06830, Turkey., Özdemir Ç; Department of Anesthesiology and Reanimation, Faculty of Medicine, Gazi University, Ankara 06510, Turkey., Kılıç Y; Department of Pediatric Cardiovascular Surgery, Gazi Yaşargil Education Research Hospital, Diyarbakır 21010, Turkey., Dursun AD; Department of Physiology, Faculty of Medicine, Atılım University, Ankara 06830, Turkey., Bostancı H; Department of General Surgery, Faculty of Medicine, Gazi University, Ankara 06510, Turkey., Kip G; Department of Anesthesiology and Reanimation, Faculty of Medicine, Gazi University, Ankara 06510, Turkey., Arslan M; Life Sciences Application and Research Center, Gazi University, Ankara 06830, Turkey.; Laboratory Animal Breeding and Experimental Researches Center (GÜDAM), Gazi University, Ankara 06510, Turkey. |
| Abstrakt: |
Objective : Lower extremity ischemia-reperfusion injury (IRI) may occur with trauma-related vascular injury and various vascular diseases, during the use of a tourniquet, in temporary clamping of the aorta in aortic surgery, or following acute or bilateral acute femoral artery occlusion. Mitochondrial dysfunction and increased basal oxidative stress in diabetes may cause an increase in the effects of increased reactive oxygen species (ROS) and mitochondrial dysfunction due to IRI. It is of great importance to examine therapeutic approaches that can minimize the effects of IRI, especially for patient groups under chronic oxidative stress such as DM. Cerium oxide (CeO 2 ) nanoparticles mimic antioxidant enzymes and act as a catalyst that scavenges ROS. In this study, it was aimed to investigate whether CeO 2 has protective effects on skeletal muscles in lower extremity IRI in mice with streptozocin-induced diabetes. Methods : A total of 38 Swiss albino mice were divided into six groups as follows: control group (group C, n = 6), diabetes group (group D, n = 8), diabetes-CeO 2 (group DCO, n = 8), diabetes-ischemia/reperfusion (group DIR, n = 8), and diabetes-ischemia/reperfusion-CeO 2 (group DIRCO, n = 8). The DCO and DIRCO groups were given doses of CeO 2 of 0.5 mg/kg intraperitoneally 30 min before the IR procedure. A 120 min ischemia-120 min reperfusion period with 100% O 2 was performed. At the end of the reperfusion period, muscle tissues were removed for histopathological and biochemical examinations. Results : Total antioxidant status (TAS) levels were found to be significantly lower in group DIR compared with group D ( p = 0.047 and p = 0.022, respectively). In group DIRCO, total oxidant status (TOS) levels were found to be significantly higher than in group DIR ( p < 0.001). The oxidative stress index (OSI) was found to be significantly lower in group DIR compared with group DCO ( p < 0.001). Paraoxanase (PON) enzyme activity was found to be significantly increased in group DIR compared with group DCO ( p < 0.001). The disorganization and degeneration score for muscle cells, inflammatory cell infiltration score, and total injury score in group DIRCO were found to be significantly lower than in group DIR ( p = 0.002, p = 0.034, and p = 0.001, respectively). Conclusions : Our results confirm that CeO 2 , with its antioxidative properties, reduces skeletal muscle damage in lower extremity IRI in diabetic mice. |
