Antinociceptive Effect of a Novel Tosylpyrazole Compound in Mice
Autor: | Juliano Ferreira, Marcos A. P. Martins, Maribel Antonello Rubin, Rogerio V. Lourega, Cleber A. Cechinel, Sara Marchesan Oliveira, Helio G. Bonacorso, Alexandre P. Wentz, Nilo Zanatta, Gerusa Duarte Dalmolin, Ronan C. Sehnem, Camila de Campos Velho Gewehr |
---|---|
Rok vydání: | 2009 |
Předmět: |
Male
Time Factors Analgesic Administration Oral Pain Bradykinin Motor Activity Pharmacology Toxicology Body Temperature Tosyl Compounds Mice chemistry.chemical_compound Oral administration Animals Edema Medicine Intracerebroventricular route Injections Spinal Injections Intraventricular Pain Measurement Dose-Response Relationship Drug business.industry Anti-Inflammatory Agents Non-Steroidal Stomach General Medicine Carrageenan Analgesics Opioid Disease Models Animal Nociception chemistry Capsaicin Celecoxib Pyrazoles Female business medicine.drug |
Zdroj: | Basic & Clinical Pharmacology & Toxicology. 104:122-129 |
ISSN: | 1742-7843 1742-7835 |
DOI: | 10.1111/j.1742-7843.2008.00353.x |
Popis: | Pain 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. |
Databáze: | OpenAIRE |
Externí odkaz: |