Navegando por Palavras-chave "Indomethacin"
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- ItemSomente MetadadadosCyclooxygenase-independent mechanism of ibuprofen-induced antipyresis: the role of central vasopressin V-1 receptors(Wiley-Blackwell, 2011-12-01) Soares, Denis M.; Cristofoletti, Rodrigo; Melo, Miriam C. C.; Lindsey, Charles Julian [UNIFESP]; Veiga-Souza, Fabiane H.; Fabricio, Aline S. C.; Souza, Gloria E. P.; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)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(CH2)(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.
- ItemAcesso aberto (Open Access)Effect of cyclooxygenase inhibitors on gentamicin-induced nephrotoxicity in rats(Associação Brasileira de Divulgação Científica, 2004-07-01) Hosaka, E.m.; Santos, Oscar Fernando Pavão dos [UNIFESP]; Seguro, A.c.; Vattimo, M.f.f.; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)The frequent use of nonsteroidal anti-inflammatory drugs (NSAID) in combination with gentamicin poses the additional risk of nephrotoxic renal failure. Cyclooxygenase-1 (COX-1) is the main enzyme responsible for the synthesis of renal vasodilator prostaglandins, while COX-2 participates predominantly in the inflammatory process. Both are inhibited by non-selective NSAID such as indomethacin. Selective COX-2 inhibitors such as rofecoxib seem to have fewer renal side effects than non-selective inhibitors. The objective of the present study was to determine whether the combined use of rofecoxib and gentamicin can prevent the increased renal injury caused by gentamicin and indomethacin. Male Wistar rats (250-300 g) were treated with gentamicin (100 mg/kg body weight, ip, N = 7), indomethacin (5 mg/kg, orally, N = 7), rofecoxib (1.4 mg/kg, orally, N = 7), gentamicin + rofecoxib (100 and 1.4 mg/kg, respectively) or gentamicin + indomethacin (100 and 5 mg/kg, respectively, N = 8) for 5 days. Creatinine clearance and alpha-glutathione-S-transferase concentrations were used as markers of renal injury. Animals were anesthetized with ether and sacrificed for blood collection. The use of gentamicin plus indomethacin led to worsened renal function (0.199 ± 0.019 ml/min), as opposed to the absence of a nephrotoxic effect of rofecoxib when gentamicin plus rofexicob was used (0.242 ± 0.011 ml/min). These results indicate that COX-2-selective inhibitors can be used as an alternative treatment to conventional NSAID, especially in situations in which risk factors for nephrotoxicity are present.
- ItemAcesso aberto (Open Access)Functional expression of kinin B1 and B2 receptors in mouse abdominal aorta(Associação Brasileira de Divulgação Científica, 2007-05-01) Felipe, Sandra Arantes [UNIFESP]; Rodrigues, Eliete da Silva [UNIFESP]; Martin, Renan Paulo [UNIFESP]; Paiva, Antonio Cechelli de Mattos [UNIFESP]; Pesquero, João Bosco [UNIFESP]; Shimuta, Suma Imura [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Previous studies have shown that the vascular reactivity of the mouse aorta differs substantially from that of the rat aorta in response to several agonists such as angiotensin II, endothelin-1 and isoproterenol. However, no information is available about the agonists bradykinin (BK) and DesArg9BK (DBK). Our aim was to determine the potential expression of kinin B1 and B2 receptors in the abdominal mouse aorta isolated from C57BL/6 mice. Contraction and relaxation responses to BK and DBK were investigated using isometric recordings. The kinins were unable to induce relaxation but concentration-contraction response curves were obtained by applying increasing concentrations of the agonists BK and DBK. These effects were blocked by the antagonists Icatibant and R-715, respectively. The potency (pD2) calculated from the curves was 7.0 ± 0.1 for BK and 7.3 ± 0.2 for DBK. The efficacy was 51 ± 2% for BK and 30 ± 1% for DBK when compared to 1 µM norepinephrine. The concentration-dependent responses of BK and DBK were markedly inhibited by the arachidonic acid inhibitor indomethacin (1 µM), suggesting a mediation by the cyclooxygenase pathway. These contractile responses were not potentiated in the presence of the NOS inhibitor L-NAME (1 mM) or endothelium-denuded aorta, indicating that the NO pathway is not involved. We conclude that the mouse aorta constitutively contains B1 and B2 subtypes of kinin receptors and that stimulation with BK and DBK induces contractile effect mediated by endothelium-independent vasoconstrictor prostanoids.
- ItemAcesso aberto (Open Access)Indomethacin can downregulate the levels of inflammatory mediators in the hippocampus of rats submitted to pilocarpine-induced status epilepticus(Faculdade de Medicina / USP, 2014-09-01) Vieira, Michele Juliane [UNIFESP]; Perosa, Sandra Regina [UNIFESP]; Argañaraz, Gustavo Adolfo [UNIFESP]; Silva Junior, Jose Antonio [UNIFESP]; Cavalheiro, Esper Abrão [UNIFESP]; Naffah-Mazzacoratti, Maria da Graca [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Sociedade Beneficente Israelita Brasileira Hospital Albert Einstein Neurofisiologia Clínica; Universidade de Brasília Faculdade de Ciências da Saúde Laboratório de Patologia Molecular; Universidade Nove de Julho Departamento de Educação Física Programa de Pós-Graduação em Ciências da ReabilitaçãoOBJECTIVE: Refractory status epilepticus is one of the most life-threatening neurological emergencies and is characterized by high morbidity and mortality. Additionally, the use of anti-inflammatory drugs during this period is very controversial. Thus, this study has been designed to analyze the effect of a low dose of indomethacin (a COX inhibitor) on the expression of inflammatory molecules.METHOD: The hippocampus of rats submitted to pilocarpine-induced long-lasting status epilepticus was analyzed to determine the expression of inflammatory molecules with RT-PCR and immunohistochemistry.RESULTS: Compared with controls, reduced levels of the kinin B2 receptors IL1β and TNFα were found in the hippocampus of rats submitted to long-lasting status epilepticus and treated with indomethacin.CONCLUSIONS: These data show that low doses of indomethacin could be employed to minimize inflammation during long-lasting status epilepticus.
- ItemSomente MetadadadosParticipation of corticosteroids and effects of indomethacin on the acute inflammatory response of rats fed n-6 or n-3 polyunsaturated fatty acid-rich diets(Kluwer Academic/plenum Publ, 2003-02-01) Wohlers, Marta [UNIFESP]; Nascimento, Claudia Maria da Penha Oller do [UNIFESP]; Xavier, Roberta Araújo Navarro [UNIFESP]; Ribeiro, Eliane Beraldi [UNIFESP]; Silveira, Vera Lucia Flor [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)We have previously shown that both n-3 (fish oil) and n-6 (soybean oil) PUFA-rich diets reduce carrageenan-induced paw edema in rats. the present study evaluated the role of corticosteroids, and the effect of indomethacin on this response. Basal (pre-carrageenan) levels of corticosterone were elevated in both lipid diets compared to the chow diet. During inflammation, corticosterone levels increased to a similar extent in the chow and lipid diets. With 2.0 mg/kg indomethacin, edema was reduced in the chow diet and the n-3 diet, while it was not changed in the n-6 diet. in contrast, the 16.6 mg/kg dose of indomethacin induced a mild increase in edema in the chow diet but a pronounced edema increase in the lipid diets. the increase in corticosterone levels induced by carrageenan was either reduced (chow) or completely abolished (lipids) by the treatment with the higher dose of indomethacin, compared to both the control (untreated) group, and the lower dose of indomethacin. These data indicate that both acute inflammation and the response to an antiinflammatory drug were attenuated by n-3 or n-6 PUFA-rich diets. They also showed that indomethacin can have anti- or proinflammatory properties reflecting the extent of the corticosterone inhibition by indomethacin.
- ItemSomente MetadadadosSleep alterations in an experimental orofacial pain model in rats(Elsevier B.V., 2003-12-12) Schütz, Teresa Cristina Barros [UNIFESP]; Andersen, Monica Levy [UNIFESP]; Tufik, Sergio [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)This study sought to assess sleep patterns in rats injected with Freund's adjuvant (FA) in the temporomandibular joint (TMJ) as a potential experimental orofacial pain model. Pain response to indomethacin was also assessed. Rats were implanted with electrodes to record electrocorticogram and eletromyogram signals. After a baseline (13) recording, they were injected with Freund's adjuvant (orofacial pain group, n = 8) or saline (sham group, n = 8) in the temporomandibular joint, and their sleep was monitored over two 12-h light periods. in the second phase of the study, after injecting Freund's adjuvant, indomethacin was administered (1 mg/kg p.o.) at 12- intervals, and sleep patterns were recorded for two additional light periods. the orofacial pain group showed a reduction in sleep efficiency during the two light periods compared with the baseline recording and with the sham group (p<0.001): Increases in sleep and paradoxical sleep (PS) latencies of approximately 200% and 420%, respectively, were observed, as well as an increase in the number of awakenings during both periods (p<0.001). Treatment with indomethacin increased sleep efficiency (p<0.001) and paradoxical sleep time (p<0.001). the number of awakenings (p<0.001) and sleep (p<0.001) and paradoxical sleep latencies (p<0.001) were reduced reestablishing the normal sleep pattern. the results showed the reliability and usefulness of the temporomandibular joint pain model to characterize sleep disturbances related to pain and its response to indomethacin.