Constantinos G Zografos1,2, Dimosthenis Chrysikos1,2, Theodoros Pittaras1,3, Vasileios Karampelias4, Aikaterini Chairakakis1, Antonis Galanos1, Ioannis Sfiniadakis5, Evangelos Felekouras6, George C Zografos2, Michail Sideris7, Konstantina Papadopoulou1, Apostolos E Papalois8,9. 1. Experimental, Educational and Research Center ELPEN, Athens, Greece. 2. 1 Department of Propaedeutic Surgery, Hippokration Hospital, Athens, Greece. 3. Hematology Laboratory - Blood Bank, National and Kapodistrian University of Athens School of Medicine, Aretaieion Hospital, Athens, Greece. 4. School of Medicine, University of Patras, Patras, Greece. 5. Pathology Laboratory, Athens Naval Hospital, Athens, Greece. 6. First Department of Surgery, Laikon General Hospital, National and Kapodistrian University of Athens, Athens, Greece. 7. Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, U.K. 8. Experimental, Educational and Research Center ELPEN, Athens, Greece apapalois@elpen.gr. 9. School of Medicine, European University Cyprus, Nicosia, Cyprus.
Abstract
BACKGROUND/AIM: U-74389G and ascorbic acid protect the cells from oxidation. This study aimed to depict their role in ischemia-reperfusion injury in a renal rat model. MATERIALS AND METHODS: Sixty Wistars rats were randomized into six groups of 10 animals each. Group A Ischemia 30 min, reperfusion 60 min; Group B Ischemia 30 min, reperfusion 120 min; Group C Ischemia 30 min, ascorbic acid administration, reperfusion 60 min; Group D Ischemia 30 min, ascorbic acid administration, reperfusion 120 min; Group E Ischemia 30 min, U-74389G administration, reperfusion 60 min; Group F Ischemia 30 min, U-74389G administration, reperfusion 120 min. We then collected tissue and blood samples. RESULTS: Histology and the significantly decreased malondialdehyde and tumor necrosis factor-α levels indicated that ascorbic acid was superior to U-74389G, at pre-defined time intervals. CONCLUSION: Ascorbic acid and U-74389G ameliorated renal damage induced by ischemia-reperfusion injury, suggesting a therapeutic effect. Copyright
BACKGROUND/AIM: U-74389G and ascorbic acid protect the cells from oxidation. This study aimed to depict their role in ischemia-reperfusion injury in a renal rat model. MATERIALS AND METHODS: Sixty Wistars rats were randomized into six groups of 10 animals each. Group A Ischemia 30 min, reperfusion 60 min; Group B Ischemia 30 min, reperfusion 120 min; Group C Ischemia 30 min, ascorbic acid administration, reperfusion 60 min; Group D Ischemia 30 min, ascorbic acid administration, reperfusion 120 min; Group E Ischemia 30 min, U-74389G administration, reperfusion 60 min; Group F Ischemia 30 min, U-74389G administration, reperfusion 120 min. We then collected tissue and blood samples. RESULTS: Histology and the significantly decreased malondialdehyde and tumor necrosis factor-α levels indicated that ascorbic acid was superior to U-74389G, at pre-defined time intervals. CONCLUSION:Ascorbic acid and U-74389G ameliorated renal damage induced by ischemia-reperfusion injury, suggesting a therapeutic effect. Copyright
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