The protective effect of oxytocin on renal ischemia/reperfusion injury in rats

• Published in: Regulatory peptides Vol. 140; no. 3; pp. 101 - 108
• Main Authors: Tuğtepe, Halil, Şener, Göksel, Bıyıklı, Neşe Karaaslan, Yüksel, Meral, Çetinel, Şule, Gedik, Nursal, Yeğen, Berrak Ç.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier B.V 03-05-2007; Amsterdam Elsevier
• Subjects: Animals; Biological and medical sciences; Cardiology. Vascular system; Creatinine - blood; Disease Models, Animal; Fundamental and applied biological sciences. Psychology; Glutathione; Glutathione - metabolism; Ischemia/reperfusion; Kidney; Kidney - drug effects; Kidney - metabolism; Kidney - pathology; Kidney Diseases - prevention & control; L-Lactate Dehydrogenase - blood; Lipid peroxidation; Male; Malondialdehyde - metabolism; Medical sciences; Myeloperoxidase; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; Oxytocin; Oxytocin - therapeutic use; Peroxidase - metabolism; Protective Agents - therapeutic use; Rats; Rats, Wistar; Reactive Oxygen Species - metabolism; Renovascular diseases; Reperfusion Injury - prevention & control; Tumor Necrosis Factor-alpha - blood; Urea - blood; Vertebrates: endocrinology; Lipid peroxidation; Myeloperoxidase; Oxytocin; Ischemia/reperfusion; Kidney; Glutathione; Kidney disease; Urinary system disease; Rat; Enzyme; Ischemia reperfusion; Rodentia; Cardiovascular disease; Lipids; Vertebrata; Mammalia; Peroxidases; Animal; Peroxidase; Oxidoreductases; Renal ischemia reperfusion injury; Peroxidation
• ISSN: 0167-0115; 1873-1686
• DOI: 10.1016/j.regpep.2006.11.026

Oxytocin was previously shown to have anti-inflammatory effects in different inflammation models. The major objective of the present study was to evaluate the protective role of oxytocin (OT) in protecting the kidney against ischemia/reperfusion (I/R) injury.
Male Wistar albino rats (250–300 g) were unilaterally nephrectomized, and subjected to 45 min of renal pedicle occlusion followed by 6 h of reperfusion. OT (1 mg/kg, ip) or vehicle was administered 15 min prior to ischemia and was repeated immediately before the reperfusion period. At the end of the reperfusion period, rats were decapitated and kidney samples were taken for histological examination or determination of malondialdehyde (MDA), an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration. Creatinine and urea concentrations in blood were measured for the evaluation of renal function, while TNF-α and lactate dehydrogenase (LDH) levels were determined to evaluate generalized tissue damage. Formation of reactive oxygen species in renal tissue samples was monitored by chemiluminescence technique using luminol and lucigenin probes.
The results revealed that I/R injury increased (
p
<
0.01–0.001) serum urea, creatinine, TNF-α and LDH levels, as well as MDA, MPO and reactive oxygen radical levels in the renal tissue, while decreasing renal GSH content. However, alterations in these biochemical and histopathological indices due to I/R injury were attenuated by OT treatment (
p
<
0.05–0.001).
Since OT administration improved renal function and microscopic damage, along with the alleviation of oxidant tissue responses, it appears that oxytocin protects renal tissue against I/R-induced oxidative damage.