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Investigation of the effects of oxytocin on oxidative stress markers, inflammatory cytokines, and prostaglandin E2 levels in the renal tissue of male rats with acute kidney injury induced by ischemia/reperfusion
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Zahra Jalali   , Mehri Kadkhodaee , Behjat Seifi , Ghorbangol Ashabi , Leila Hafazeh , Nasim Aminaie , Mina Ranjbaran *  |
| Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran |
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Abstract: (16 Views) |
Background and Aim: Renal ischemia/reperfusion injury is a major cause of acute kidney injury (AKI) and is associated with increased production of reactive oxygen species (ROS), lipid peroxidation, and inflammatory responses. Oxytocin, a hypothalamic nanopeptide, has been reported to possess anti-inflammatory and antioxidant properties in addition to its classical physiological functions. One potential mechanism underlying the protective effects of oxytocin is the enhancement of prostaglandin E2 (PGE2) production, which may protect renal tissue by reducing oxidative stress and suppressing inflammation. Therefore, this study aimed to investigate the effects of oxytocin on renal function, oxidative stress, inflammatory cytokines, and PGE2 levels in an experimental model of renal ischemia/reperfusion injury.
Methods: Eighteen male Wistar rats (250–300 g) were randomly assigned to three groups: Sham (surgery without renal pedicle occlusion), Ischemia/reperfusion (bilateral renal artery ischemia for 45 min followed by 48 h of reperfusion), and Ischemia/reperfusion + Oxytocin (same procedure as the Ischemia/reperfusion group, with intraperitoneal administration of oxytocin at a dose of 0.4 μg/kg immediately after ischemia). After 48 h, serum samples were collected for assessment of renal function indices (BUN and creatinine). Renal tissue samples were analyzed for oxidative stress markers [malondialdehyde (MDA) and superoxide dismutase (SOD)], inflammatory cytokines (TNF-α and IL-6), PGE2 levels, and histopathological alterations.
Results: Renal ischemia/reperfusion significantly increased MDA, TNF-α, IL-6, and PGE2 levels while significantly reducing SOD activity compared with the Sham group. Oxytocin treatment further increased PGE2 levels and SOD activity and significantly reduced MDA and inflammatory cytokine levels compared with the Ischemia/reperfusion group.
Conclusion: Oxytocin attenuates oxidative stress and inflammation in renal ischemia/reperfusion -induced acute kidney injury. These protective effects may be mediated not only through direct suppression of ROS generation but also through increased PGE2 production and activation of its receptors, leading to enhanced antioxidant defense, reduced inflammation, and improved renal hemodynamics. |
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| Keywords: Oxidative Stress, Oxytocin, Inflammation, Ischemia/Reperfusion, Prostaglandin E2, Acute Kidney Injury |
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Full-Text [PDF 1186 kb]
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Type of Study: Original Research |
Subject:
Kidney and Urinary tracts
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