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1 Departamento Fisiologia, Universidad Complutense, Madrid, Spain
2 Departamento Ciencias Morfologicas y Fisiologia, Universidad Europea, Madrid, Spain
* To whom correspondence should be addressed. E-mail: ALC{at}med.ucm.es.
Chronic arthritis induces hypermetabolism and cachexia. Ghrelin is a gastrointestinal hormone that has been proposed as a treatment to prevent cachexia. The aim of this work was to examine the effect of administration of the ghrelin agonist, GHRP-2, to arthritic rats. Male Wistar rats were injected with Freund's adjuvant and 15 days later, arthritic and control rats were daily injected with GHRP-2 (100 µg/kg) or with saline, for 8 days. Arthritis induced an increase in serum ghrelin (P<0.01) and a decrease in serum concentrations of leptin (P<0.01) whereas GHRP-2 administration increased serum concentrations of leptin. GHRP-2 increased food intake in control rats, but not in arthritic rats. However, in arthritic rats GHRP-2 administration ameliorated the external symptoms of arthritis, since it decreased the arthritis score (10.4 ± 0.8 vs. 13.42 ± 0.47; P<0.01) and the paw volume. In addition, circulating interleukin-6 (IL-6) and nitrites/nitrates were increased by arthritis, and GHRP-2 treatment decreased the serum IL-6 levels (P<0.01). In order to elucidate whether GHRP-2 is able to modulate IL-6 release directly on immune cells, peritoneal macrophage cultures were incubated with GHRP-2 or ghrelin, the endogenous ligand of the growth hormone (GH) secretagogue receptor. Both GHRP-2 (10-7 M) and ghrelin (10-7 M) prevented endotoxin-induced IL-6 and decreased nitrite/nitrate release from peritoneal macrophages "in vitro". These data suggest that GHRP-2 administration has an anti-inflammatory effect in arthritic rats that seems to be mediated by ghrelin receptors directly on immune cells.
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