Major Ozonated Autohemotherapy Preconditioning Ameliorates Kidney Ischemia-Reperfusion Injury.
Medical ozone has therapeutic properties as an antimicrobial, anti-inflammatory, modulator of antioxidant defense system. Major ozonated autohemotherapy (MOA) is a new therapeutic approach that is widely used in the treatment of many diseases. The objective of the present study was to determine whether preischemic application of MOA would attenuate renal ischemia-reperfusion injury (IRI) in rabbits. Twenty-four male New Zealand white rabbits were divided into four groups, each including six animals: (1) Sham-operated group, (2) Ozone group (the MOA group without IRI), (3) IR group (60 min ischemia followed by 24 h reperfusion), and (4) IR + MOA group (MOA group). The effects of MOA were examined by use of hematologic and biochemical parameters consisting of neutrophil to lymphocyte ratio (NLR), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), ischemia-modified albumin (IMA), total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI). In addition, the histopathological changes including the tubular brush border loss (TBBL), tubular cast (TC), tubular necrosis (TN), intertubular hemorrhage and congestion (IHC), dilatation of bowman space (DBS), and interstitial inflammatory cells infiltration (IECI) were evaluated. In the IR group, compared to the Sham group, biochemical parameters indicating oxidative stress, NLR, IL-6, TNF-α, IMA, TOS, and OSI have increased. MOA reduced inflammation and oxidative stress parameters. Although TAS values have decreased in the IR group and increased in the MOA-pretreated group, no significant changes in TAS values were detected between the IR and MOA groups. The total score was obtained by summing all the scores from morphological kidney damage markers. The total score has increased with IR damage when compared with the Sham group (13.83 ± 4.30 vs 1.51 ± 1.71; p = 0.002). But, the total score has decreased significantly after application of MOA (5.01 ± 1.49; p = 0.002; compared with the IR group). MOA preconditioning is effective in reducing tissue damage induced in kidney ischemia-reperfusion injury. The protective effect of MOA is mediated via reducing inflammatory response and regulating of reactive oxygen species (ROS). Renal histology also showed convincing evidence regarding MOA's protective nature against kidney injury induced renal ischemia-reperfusion. Consequently, MOA might be helpful in protecting the kidneys from IR-induced damage in humans, probably through the anti-inflammatory effect and reducing the total oxidant status.
Department of Urology, Canakkale Onsekiz Mart University, Faculty of Medicine, Canakkale, Turkey. eyupburaksancak@comu.edu.tr.|Canakkale Onsekiz Mart Universitesi, Terzioglu Yerleskesi, Barbaros Mh, 17100, Canakkale, Turkey. eyupburaksancak@comu.edu.tr.
Eyup Burak
EB
Sancak
Department of Biochemistry, Canakkale Onsekiz Mart University, Faculty of Medicine, Canakkale, Turkey.
Hakan
H
Turkön
Department of Pathology, Abant Izzet Baysal University, Faculty of Medicine, Bolu, Turkey.
Selma
S
Çukur
Department of Histology and Embryology, Abant Izzet Baysal University, Faculty of Medicine, Bolu, Turkey.
Sevilay
S
Erimsah
Department of Urology, Canakkale Onsekiz Mart University, Faculty of Medicine, Canakkale, Turkey.
Alpaslan
A
Akbas
Department of Urology, Canakkale Onsekiz Mart University, Faculty of Medicine, Canakkale, Turkey.
Murat Tolga
MT
Gulpinar
Department of Anesthesiology, Canakkale Onsekiz Mart University, Faculty of Medicine, Canakkale, Turkey.
Huseyin
H
Toman
Department of Anesthesiology, Canakkale Onsekiz Mart University, Faculty of Medicine, Canakkale, Turkey.
Hasan
H
Sahin
Department of Physiology, Canakkale Onsekiz Mart University, Faculty of Medicine, Canakkale, Turkey.
Metehan
M
Uzun
D058186:Acute Kidney Injury / Q000188:drug therapy / Q000517:prevention & control*; D000818:Animals; D015415:Biomarkers; D007249:Inflammation / Q000188:drug therapy* / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology; D008297:Male; D009504:Neutrophils / Q000276:immunology; D010083:Oxidants, Photochemical / Q000627:therapeutic use*; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects; D010126:Ozone / Q000627:therapeutic use*; D011817:Rabbits; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000188:drug therapy / Q000517:prevention & control*; D012709:Serum Albumin / Q000276:immunology; D000075462:Serum Albumin, Human; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
D015415:Biomarkers; D015850:Interleukin-6; D010083:Oxidants, Photochemical; D017382:Reactive Oxygen Species; D012709:Serum Albumin; D014409:Tumor Necrosis Factor-alpha; C561522:ischemia-modified albumin; D010126:Ozone; D000075462:Serum Albumin, Human
major ozonated autohemotherapy; medical ozone; neutrophil to lymphocyte ratio; renal ischemia-reperfusion injury; total oxidant status