Oxytocin ameliorates skin damage and oxidant gastric injury in rats with thermal trauma

Abstract Transient splanchnic vasoconstriction following major burns causes oxidative and/or nitrosative damage in gastrointestinal tissues due to ischemia, which is followed by reperfusion injury. Oxytocin (OT), a hypothalamic nonapeptide, possesses antisecretory and antiulcer effects, facilitates wound healing and is involved in immune and inflammatory processes. To assess the possible protective effect of oxytocin (OT) against burn-induced gastric injury, Sprague–Dawley rats (250–300 g) were randomly divided into three groups as control ( n  = 8), OT-treated burn ( n  = 8) and saline-treated burn ( n  = 8) groups. Under anesthesia, the shaved dorsal skin of rats was exposed to 90 °C water for 10 s to induce burn injury covering 30% of total body surface area in a standardized manner. Either oxytocin (5 μg/kg) or saline was administered subcutaneously immediately after and at 24 h following burn, and the rats were decapitated at 48 h. Serum samples were assayed for TNF-alpha, and stomach was taken for the determination of malondialdehyde (MDA), myeloperoxidase (MPO) activity, DNA fragmentation rate (%) and histopathological examination. MDA and MPO were assayed for products of lipid peroxidation and as an index of tissue neutrophil infiltration, respectively. When compared to control group, burn caused significant increases in gastric MDA and MPO activity and increased microscopic damage scores at 48 h ( p p p p p