Abstract
Oxytocin (OT), a neurohypophysial nonapeptide, plays dual role as a neurotransmitter/neuromodulator and a hormone. It has also well known protective properties against ischemia/reperfusion organ damage. This study investigated the effect of OT on experimentally induced ovarian torsion/de-torsion ischemia/reperfusion (I/R) injury in rats. Sprague-Dawley rats were assigned to five treatment groups (n=7/group): Group 1, sham-operated; Group 2, torsion; Group 3, 80IU/kg of OT administration 30min prior to torsion; Group 4, torsion/de-torsion; and Group 5, torsion followed by 80IU/kg of OT administration 30min prior to de-torsion. OT administration significantly decreased the tissue malondialdehyde (MDA) levels in both the torsion and OT group (Group 3), and torsion/de-torsion OT group (Group 5) in comparison with the torsion-only group (Group 2) and torsion/de-torsion group (Group 4). Histopathological finding scores including follicular degeneration, edema, hemorrhage, vascular congestion, and infiltration by inflammatory cells were found to be significantly decreased in the torsion and OT group (Group 3), and torsion/de-torsion OT group (Group 5) when compared with the torsion-only group (Group 2) and torsion/de-torsion group (Group 4). In conclusion, these results, verified with histopathologic evaluation and biochemical assays, suggest a probable protective role for OT in ischemia and I/R injury in rat ovaries.
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