Effects of Enrofloxacin, Flunixin and Dexamethasone on Indicators of Oxidative and Organ Damage in Lipopolysaccharide-Induced Endotoxemia

The aim of this study was to determine the effects of enrofloxacin, flunixin meglumine and dexamethasone on antioxidant status and markers of organ damage in endotoxemia. Rats were divided into four groups. The groups received the following drugs (simultaneously with lipopolysaccharide): enrofloxacin, flunixin meglumine, low-dose dexamethasone or high-dose dexamethasone, respectively. After the treatments, serum and plasma samples were collected at 1, 2, 4, 6, 8, 12, 24 and 48 h. The levels of malondialdehyde, nitric oxide, superoxide dismutase, vitamin C and 13,14-dihydro-15-keto-prostaglandin F2α were determined with ELISA. The cardiac, hepatic and renal damage markers were measured with autoanalyzer. Elevated levels of malondialdehyde were relatively inhibited by high-dose dexamethasone. Increases in the levels of nitric oxide were inhibited by low and high-dose dexamethasone while increases in the level of 13,14-dihydro-15-keto prostaglandin F2α were inhibited by all treatments except enrofloxacin. No treatments inhibited the decrease in vitamin C levels. Cardiac and hepatic damage was not inhibited completely whereas renal damage was inhibited by treatment with low or high-dose dexamethasone. The results show that although low-dose dexamethasone had antioxidant activity and protected against organ damage, high-dose dexamethasone may be more beneficial in the treatment of endotoxemia.