Özet:
Background. Thermal injury causes a breakdown in the
intestinal mucosal barrier due to ischemia reperfusion
injury, which can induce bacterial translocation (BT), sepsis,
and multiple organ failure in burn patients. The aim of
this study was to investigate the effect of ethyl pyruvate
(EP) on intestinal oxidant damage and BT in burn injury.
Materials and methods. Thirty-two rats were randomly
divided into four groups. The sham group was
exposed to 21°C water and injected intraperitoneal with
saline (1 mL/100 g). The sham EP group received EP
(40 mg/kg) intraperitoneally 6 h after the sham procedure.
The burn group was exposed to thermal injury and
given intraperitoneal saline injection (1 mL/100 g). The
burn EP group received EP (40 mg/kg) intraperitoneally
6 h after thermal injury. Twenty-four hours later,
tissue samples were obtained from mesenteric lymph
nodes, spleen, and liver for microbiological analysis and
ileum samples were harvested for biochemical analysis.
Results. Thermal injury caused severe BT in burn
group. EP supplementation decreased BT in mesenteric
lymph nodes and spleen in the burn EP group compared
with the burn group (P < 0.05). Also, burn caused
BT in liver, but this finding was not statistically signifi-
cant among all groups. Thermal injury caused a statistically
significant increase in malondialdehyde and myeloperoxidase
levels, and EP prevented this effects in the
burn EP group compared with the burn group (P < 0.05).
Conclusion. Our data suggested that EP can inhibit
the BT and myeloperoxidase and malondialdehyde
production in intestine following thermal injury, suggesting
anti-inflammatory and anti-oxidant properties
of EP.
