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1 Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, University of Sao Paulo, Ribeirao Preto, SP, Brazil; Institute of Pharmacology, Catholic University Medical School, Rome, RM, Italy
2 Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, University of Sao Paulo, Ribeirao Preto, SP, Brazil
3 Institute of Pharmacology, Catholic University Medical School, Rome, RM, Italy
* To whom correspondence should be addressed. E-mail: alinefabricio{at}hotmail.com.
It was previously shown that sustained fever can be induced in rats by central injection of endothelin-1 (ET-1). This peptide appears to participate into the mechanism(s) of lipopolysaccharide (LPS)-induced fever, which is reduced by pre-treatments with ETB receptor antagonists. In this study we compared the effects of a non-selective cyclo-oxygenase (COX) inhibitor, indomethacin, with those of two selective COX-2 inhibitors, celecoxib and lumiracoxib, on ET-1-induced fever in rats. Fever induced in conscious animals by ET-1 (1 pmol, i.c.v.) or LPS (5 µg kg-1, i.v.) was prevented by pre-treatments with celecoxib (5 and 10 mg kg-1) or lumiracoxib (5 mg kg-1), given by oral gavage 1 h before stimuli. Lower doses of celecoxib had partial (2.5 mg kg-1) or no effect (1 mg kg-1). Indomethacin (2 mg kg-1, i.p.) partially inhibited fever induced by LPS but had no effect on ET-1-induced fever. The levels of prostaglandin(PG)E2 and PGF2
in the cerebrospinal fluid (CSF) of pentobarbital-anesthetized rats were significantly increased 3 h after the injection of LPS or ET-1. The latter increase was abolished by celecoxib at all tested doses and by indomethacin. In conclusion, selective COX-2 inhibitors were able to prevent ET-1-induced fever, indicating a role for COX-2 in this phenomenon. However, the fact that reduced CSF PGs levels obtained with indomethacin and a low dose of celecoxib are not accompanied by changes in fever induced by ET-1, along with the lack of inhibitory effects of indomethacin on ET-1 fever, suggest that the latter might also involve COX-2-independent mechanisms.
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