Study of illness anorexia in birds by concentrating on roles of central and peripheral cyclooxygenases-1 and cyclooxygenases-2

Abstract

Prostaglandin E2 (PGE2) is one of the major mediators involved in illness anorexia in rodents. Cyclooxygenases (COX), the important enzymes in prostaglandin synthesizing pathway, have two main isoforms named COX-1 and COX-2. Lipopolysaccharides (LPS) are components of the cell wall of gram-negative bacteria which are used as a standard model of infection. Here, we evaluated the interaction between central and peripheral COX-1 and COX-2 with LPS in neonatal broilers. In the central experiments, the following drugs were injected intracerebroventricularly (ICV): LPS (100 ng), piroxicam, a selective inhibitor of COX-1 (10, 50, 100 μg), nimesulide, a selective inhibitor of COX-2 (1, 5, 10, 20 μg), and LPS plus piroxicam and LPS plus nimesulide (100 ng and 50 μg, respectively). For peripheral experiments, either the solvent or LPS were injected intraperitoneally 30 min after piroxicam or nimesulide administration. Food intake was assessed at 30 to 360 min post-injections in 3 h fasted chicks. In both central and peripheral administrations, LPS, piroxicam, and nimesulide either alone or in combination suppressed food intake. Injection of LPS plus COX-1 and COX-2 inhibitors also exacerbated food intake suppression. Our results showed that COXs are not involved in the illness anorexia in neonatal chicks. The other pathways such as Cox-PGD2 might be involved and requires more studies. It seems that administration of COXs inhibitors such as aspirin or indomethacin might not recommended for improvement of the illness anorexia in infectious diseases of neonatal chicks.

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