Nimesulide-induced antipyresis in rats involves both cyclooxygenase-dependent and independent mechanisms

Maria F.P. Werner; Glória E.P. Souza; Aleksander R. Zampronio

doi:10.1016/j.ejphar.2006.05.029

Nimesulide-induced antipyresis in rats involves both cyclooxygenase-dependent and independent mechanisms

Maria F.P. Werner, Glória E.P. Souza, Aleksander R. Zampronio

Research output: Contribution to journal › Article › peer-review

11 Citations (Scopus)

Abstract

This study evaluates the antipyretic activity of nimesulide, a cyclooxygenase (COX-2) selective inhibitor in rats. The effects of nimesulide on lipopolysaccharide (LPS)-induced cerebrospinal prostaglandin E₂ (PGE₂) and prostaglandin F_2α (PGF_2α) and on plasma tumor necrosis factor-α (TNF-α) levels were also evaluated. Male Wistar rats received an i.p. injection of LPS, or i.c.v. injections of interleukin-1β (IL-1β), interleukin-6 (IL-6), TNF-α, macrophage inflammatory protein-1α (MIP-1α), arachidonic acid, PGE₂, PGF_2α, corticotrophin-releasing factor (CRF) or endothelin-1 (ET-1). Nimesulide or indomethacin administered i.p 30 min prior LPS, IL-1β, IL-6, TNF-α or arachidonic acid reduced the febrile response and PGE₂ or PGF_2α levels in LPS-febrile rats but did not modify PGE₂-induced fever. Nimesulide, but not indomethacin, reduced the fever induced by MIP-1α, PGF_2α, CRF or ET-1. Plasma TNF-α levels in LPS-treated rats were also reduced by nimesulide. These findings confirm that the antipyretic effect of nimesulide differs from the antipyretic scenario with the non-selective cyclooxygenase blocker indomethacin. Additional mechanisms, including inhibition of increased plasma TNF-α, may contribute to its antipyretic activity in rats.

Original language	English
Pages (from-to)	181-189
Number of pages	9
Journal	European Journal of Pharmacology
Volume	543
Issue number	1-3
DOIs	https://doi.org/10.1016/j.ejphar.2006.05.029
Publication status	Published - Aug 14 2006
Externally published	Yes

Bibliographical note

Funding Information:
The kind donation of nimesulide by Shering-Plough, Rio de Janeiro, Brazil, is gratefully acknowledged. The study was supported by the Conselho Nacional de Desenvolvimento Cientifico e Tecnológico (CNPq), Coordenação de Aperfeicoamento de Pessoal de Nível Superior (Capes), Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP). MFPW was the recipient of a Capes scholarship.

ASJC Scopus Subject Areas

Pharmacology

PubMed: MeSH publication types

Journal Article
Research Support, Non-U.S. Gov't

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10.1016/j.ejphar.2006.05.029

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title = "Nimesulide-induced antipyresis in rats involves both cyclooxygenase-dependent and independent mechanisms",

abstract = "This study evaluates the antipyretic activity of nimesulide, a cyclooxygenase (COX-2) selective inhibitor in rats. The effects of nimesulide on lipopolysaccharide (LPS)-induced cerebrospinal prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) and on plasma tumor necrosis factor-α (TNF-α) levels were also evaluated. Male Wistar rats received an i.p. injection of LPS, or i.c.v. injections of interleukin-1β (IL-1β), interleukin-6 (IL-6), TNF-α, macrophage inflammatory protein-1α (MIP-1α), arachidonic acid, PGE2, PGF2α, corticotrophin-releasing factor (CRF) or endothelin-1 (ET-1). Nimesulide or indomethacin administered i.p 30 min prior LPS, IL-1β, IL-6, TNF-α or arachidonic acid reduced the febrile response and PGE2 or PGF2α levels in LPS-febrile rats but did not modify PGE2-induced fever. Nimesulide, but not indomethacin, reduced the fever induced by MIP-1α, PGF2α, CRF or ET-1. Plasma TNF-α levels in LPS-treated rats were also reduced by nimesulide. These findings confirm that the antipyretic effect of nimesulide differs from the antipyretic scenario with the non-selective cyclooxygenase blocker indomethacin. Additional mechanisms, including inhibition of increased plasma TNF-α, may contribute to its antipyretic activity in rats.",

author = "Werner, {Maria F.P.} and Souza, {Gl{\'o}ria E.P.} and Zampronio, {Aleksander R.}",

note = "Funding Information: The kind donation of nimesulide by Shering-Plough, Rio de Janeiro, Brazil, is gratefully acknowledged. The study was supported by the Conselho Nacional de Desenvolvimento Cientifico e Tecnol{\'o}gico (CNPq), Coordena{\c c}{\~a}o de Aperfeicoamento de Pessoal de N{\'i}vel Superior (Capes), Funda{\c c}{\~a}o de Amparo {\`a} Pesquisa do Estado de S{\~a}o Paulo (FAPESP). MFPW was the recipient of a Capes scholarship.",

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AU - Souza, Glória E.P.

AU - Zampronio, Aleksander R.

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N2 - This study evaluates the antipyretic activity of nimesulide, a cyclooxygenase (COX-2) selective inhibitor in rats. The effects of nimesulide on lipopolysaccharide (LPS)-induced cerebrospinal prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) and on plasma tumor necrosis factor-α (TNF-α) levels were also evaluated. Male Wistar rats received an i.p. injection of LPS, or i.c.v. injections of interleukin-1β (IL-1β), interleukin-6 (IL-6), TNF-α, macrophage inflammatory protein-1α (MIP-1α), arachidonic acid, PGE2, PGF2α, corticotrophin-releasing factor (CRF) or endothelin-1 (ET-1). Nimesulide or indomethacin administered i.p 30 min prior LPS, IL-1β, IL-6, TNF-α or arachidonic acid reduced the febrile response and PGE2 or PGF2α levels in LPS-febrile rats but did not modify PGE2-induced fever. Nimesulide, but not indomethacin, reduced the fever induced by MIP-1α, PGF2α, CRF or ET-1. Plasma TNF-α levels in LPS-treated rats were also reduced by nimesulide. These findings confirm that the antipyretic effect of nimesulide differs from the antipyretic scenario with the non-selective cyclooxygenase blocker indomethacin. Additional mechanisms, including inhibition of increased plasma TNF-α, may contribute to its antipyretic activity in rats.

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ER -

Nimesulide-induced antipyresis in rats involves both cyclooxygenase-dependent and independent mechanisms

Abstract

Bibliographical note

ASJC Scopus Subject Areas

PubMed: MeSH publication types

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