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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Cyclooxygenase-independent mechanism of ibuprofen-induced antipyresis: the role of central vasopressin V-1 receptors

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Author(s):
Soares, Denis M. [1] ; Cristofoletti, Rodrigo [1] ; Melo, Miriam C. C. [1] ; Lindsey, Charles J. [2] ; Veiga-Souza, Fabiane H. [1] ; Fabricio, Aline S. C. [1] ; Souza, Gloria E. P. [1]
Total Authors: 7
Affiliation:
[1] USP, Farmacol Lab, Fac Ciencias Farmaceut Ribeirao Preto, BR-14040903 Ribeirao Preto, SP - Brazil
[2] Univ Fed Sao Paulo, Dept Biofis, Escola Paulista Med, BR-01402000 Sao Paulo - Brazil
Total Affiliations: 2
Document type: Journal article
Source: FUNDAMENTAL & CLINICAL PHARMACOLOGY; v. 25, n. 6, p. 670-681, DEC 2011.
Web of Science Citations: 4
Abstract

This study compared the antipyretic effects of ibuprofen and indomethacin regarding the efficacy in blocking fevers induced by lipopolysaccharide (LPS from E. coli) or pyrogenic mediators that act on prostaglandin (PG)-dependent and PG-independent pathways. The content of PGE(2) in the cerebrospinal fluid (CSF) and the dependence on central arginine vasopressin (AVP) release by both antipyretics were also compared during the reduction of LPS-induced fever. Finally, we investigated the effect of ibuprofen on hypothalamic cytokine content during LPS-induced fever. Ibuprofen (intraperitoneally, i.p.) dose-dependently inhibited the fever induced by LPS (intravenously, i.v.). Indomethacin (2 mg/kg) and ibuprofen (10 mg/kg) reduced the fever induced by i.c.v. injection of interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, or arachidonic acid (AA). Ibuprofen, but not indomethacin, inhibited i.c.v. endothelin-1- and pre-formed pyrogenic factor (PFPF)-induced fever. Neither ibuprofen nor indomethacin affected fever by PGE(2), PGF(2 alpha), or corticotrophin-releasing factor (CRF); however, both reduced the CSF PGE(2) content after LPS. Bilateral injection of the AVP V(1) receptor antagonist d(CH(2))(5)Tyr(Me) AVP into the ventral septal area blocked both ibuprofen- and indomethacin-induced antipyresis. Ibuprofen did not modify the hypothalamic increase in either IL-1 beta or IL-6 induced by LPS. In conclusion, although the antipyretic effect of ibuprofen involves the blockage of central production of PGE(2) and the endogenous release of AVP, differently from low dose of indomethacin, ibuprofen not only reduced the fever induced by PGE(2)-dependent, but also, that induced by PGE(2)-independent endogenous pyrogens. Moreover, ibuprofen does not affect the hypothalamic synthesis/release of IL-1 beta and IL-6. (AU)

FAPESP's process: 08/10323-3 - Investigation of the cellular and molecular mechanisms involved on fever induced by CCL3/MIP-1alpha
Grantee:Denis de Melo Soares
Support Opportunities: Scholarships in Brazil - Post-Doctoral
FAPESP's process: 99/12466-5 - Neuropeptides in Defense Responses and Homeostasis: Receptors and Neuronal Pathways
Grantee:Charles Julian Lindsey
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 97/09837-6 - Mechanisms and mediators involved in the integration of fever and inflammatory responses
Grantee:Glória Emília Petto de Souza
Support Opportunities: Research Projects - Thematic Grants