Korean J Physiol Pharmacol.  2013 Apr;17(2):169-173. 10.4196/kjpp.2013.17.2.169.

Oxytocin Ameliorates Remote Liver Injury Induced by Renal Ischemia-Reperfusion in Rats

Affiliations
  • 1Department of Pharmacology, Faculty of Medicine, Dicle University, 21280 Diyarbakir, Turkey. hakkoc@dicle.edu.tr
  • 2Department of Clinical Biochemistry, Faculty of Medicine, Dicle University, 21280 Diyarbakir, Turkey.
  • 3Department of Pathology, Faculty of Medicine, Dicle University, 21280 Diyarbakir, Turkey.

Abstract

Renal ischemia-reperfusion (IR) causes remote liver damage. Oxytocin has anti-inflammatory and antioxidant effects. The main purpose of this study was to evaluate the protective function of oxytocin (OT) in remote liver damage triggered by renal IR in rats. Twenty four rats were randomly divided into four different groups, each containing 8 rats. The groups were as follows: (1) Sham operated group; (2) Sham operated+OT group (3) Renal IR group; (4) Renal IR+OT group. OT (500microg/kg) was administered subcutaneously 12 and 24 hours before and immediately after ischemia. At the end of experimental procedure, the rats were sacrificed, and liver specimens were taken for histological assessment or determination of malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), paraoxonase (PON-1) activity and nitric oxide (NO). The results showed that renal IR injury constituted a notable elevation in MDA, TOS, Oxidative stress index (OSI) and significantly decreased TAS, PON-1 actvity and NO in liver tissue (p<0.05). Additionally renal IR provoked significant augmentation in hepatic microscopic damage scores. However, alterations in these biochemical and histopathological indices due to IR injury were attenuated by OT treatment (p<0.05). These findings show that OT ameliorates remote liver damage triggered by renal ischemia-reperfusion and this preservation involves suppression of inflammation and regulation of oxidant-antioxidant status.

Keyword

Inflammation; Ischemia-reperfusion; Oxidative stress; Oxytocin; Remote liver injury

MeSH Terms

Animals
Antioxidants
Aryldialkylphosphatase
Inflammation
Ischemia
Liver
Malondialdehyde
Nitric Oxide
Oxidative Stress
Oxytocin
Rats
Salicylamides
Antioxidants
Aryldialkylphosphatase
Malondialdehyde
Nitric Oxide
Oxytocin
Salicylamides

Figure

  • Fig. 1 Photomicrographs of Hematoxylin and Eosin stained sections from liver of rats. Minimal changes observed in sham (A) and sham+OT (B) groups. Congestion, hepatocyte vacuolization, sinusoidal dilatation, central vein dilatation, Kupffer cell activation and periportal inflammation are seen in IR group (C) sections. Histopathological alterations that were observed in IR group were significantly improved in IR+OT group (D). cv, central vein; v, vacuoles; kc, Kuppfer cells (inset); asterisk, inflammatory cells (inset); c, congestion; arrows, sinusoidal dilatation; IR, ischemia-reperfusion; OT, oxytocin.


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