Purpose: Dexamethasone has been widely used to treat acute inflammatory diseases and endotoxic shocks in animal models. Meloxicam is one of the most commonly used anti-inflammatory agents in avian species. However, little is known about the effects of dexamethasone and meloxicam on lipopolysaccharide (LPS)-induced acute inflammatory response in birds. In the present study, LPS-challenged broiler chickens were used to investigate the comparative protective effects of meloxicam and dexamethasone on LPS-induced acute inflammatory responses.
Methods: Lipopolysaccharide (LPS)-induced acute lung injury (ALI) histopathological scores, selected serum acute phase reactants, inflammatory mediators, and gangliosides were evaluated in broiler chickens inoculated with LPS and simultaneously treated with two doses of meloxicam (0.5 and 2 mg/kg BW) and dexamethasone (2 and 4 mg/kg BW).
Results: LPS-induced ALI scores were not significantly different between the meloxicam-treated, dexamethasone-treated, and untreated positive control groups at 4 hours after LPS inoculation. Interleukin-6 concentrations were also statistically the same among the positive control, dexamethasone-treated, and meloxicam-treated groups at 3 and 12 hours after LPS inoculation. However, these anti-inflammatory drugs reduced adenosine deaminase, ceruloplasmin, lipid-bound sialic acid, protein-bound sialic acid, and total sialic acid in LPS-inoculated broiler chickens at 12, 24, and 48 hours after LPS inoculation in a drug- and dose-dependent manner. Ovotransferrin concentrations were not significantly different between positive control and treatment groups at 12 hours after LPS inoculation. However, twenty-four hours after LPS inoculation, all the treated groups, except the one treated with 0.5 mg/kg meloxicam, showed significantly lower concentrations of ovotransferrin as compared with the positive control group.
Conclusion: Our results showed that dexamethasone was more effective than meloxicam in inhibiting the LPS-induced response in broiler chickens by diminishing the serum levels of adenosine deaminase, ceruloplasmin, and gangliosides.
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| http://dx.doi.org/10.2147/JIR.S258328 | DOI Listing |
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