dc.contributorFerreira, Juliano
dc.contributorhttp://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4768702Y6
dc.contributorOtuki, Michel Fleith
dc.contributorhttp://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4765550U6
dc.contributorOliveira, Mauro Schneider
dc.contributorhttp://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4705848A9
dc.creatorOliveira, Sara Marchesan de
dc.date.accessioned2017-05-02
dc.date.accessioned2019-05-24T19:13:37Z
dc.date.available2017-05-02
dc.date.available2019-05-24T19:13:37Z
dc.date.created2017-05-02
dc.date.issued2009-12-18
dc.identifierOLIVEIRA, Sara Marchesan de. Study of the analgesic and antiinflammatory potential of 3-(4-fluorophenyl)-5-trifluoromethyl-1h-1-tosylpyrazole in pain models in mice. 2009. 60 f. Dissertação (Mestrado em Bioquímica) - Universidade Federal de Santa Maria, Santa Maria, 2009.
dc.identifierhttp://repositorio.ufsm.br/handle/1/11114
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/2832709
dc.description.abstractPain is the most common complaint in the medical field and the identification of compounds that can effectively treat painful states without induction of side-effects remains a major challenge in biomedical research. The aim of the present study was to investigate the antinociceptive effect of a novel compound, 3-(4-fluorophenyl)-5-trifluoromethyl-1H-1-tosylpyrazole (compound A) in several models of pain in mice and compare with those produced by the known trifluoromethyl-containing pyrazole compound celecoxib. Compound A or celecoxib were administrated by oral (78 780 μmol/kg), intrathecal (9 22.5 nmol/site) or intracerebroventricular (9 22.5 nmol/site) routes. Oral administration of either compound A or celecoxib abolished the mechanical allodynia, but not the oedema caused by intraplantar injection of carrageenan. Similarly, compound A reduced the overt nociception, but not the oedema, produced by bradykinin or capsaicin. However, compound A (500 μmol/kg, orally) did not alter nociception nor oedema caused by intraplantar injection of prostaglandin E2 or glutamate, whereas celecoxib reduced only the nociception induced by the former. Moreover, oral and intrathecal administration of compound A or celecoxib also reduced the nociception induced by acetic acid. However, only celecoxib reduced the acetic acid-induced nociception when it was injected by the intracerebroventricular route. Finally, neither compound A nor celecoxib was able to produce antinociceptive effect in the tail-flick test or to alter the motor performance and the body temperature. Besides, compound A or celecoxib did not induce gastric lesion. Thus, compound A seems to be an interesting prototype for the development of novel analgesic drugs.
dc.publisherUniversidade Federal de Santa Maria
dc.publisherBR
dc.publisherBioquímica
dc.publisherUFSM
dc.publisherPrograma de Pós-Graduação em Ciências Biológicas: Bioquímica Toxicológica
dc.rightsAcesso Aberto
dc.subjectDor
dc.subjectNocicepção
dc.subjectInflamação
dc.subjectEdema
dc.subjectPirazóis
dc.subjectAnalgésicos
dc.subjectPain
dc.subjectNociception
dc.subjectInflammation
dc.subjectEdema
dc.subjectPyrazoles
dc.subjectAnalgesics
dc.titleEstudo do potencial analgésico e antiinflamatório do 3-(4-fluorfenil)-5-trifluormetil-1h-1-tosilpirazol em modelos de dor em camundongos
dc.typeTesis


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