dc.creatordeMello, SBV
dc.creatorNovaes, GS
dc.creatorLaurindo, IMM
dc.creatorMuscara, MN
dc.creatorMaciel, FMD
dc.creatorCossermelli, W
dc.date1997
dc.dateFEB
dc.date2014-12-16T11:34:09Z
dc.date2015-11-26T17:57:43Z
dc.date2014-12-16T11:34:09Z
dc.date2015-11-26T17:57:43Z
dc.date.accessioned2018-03-29T00:41:18Z
dc.date.available2018-03-29T00:41:18Z
dc.identifierInflammation Research. Birkhauser Verlag Ag, v. 46, n. 2, n. 72, n. 77, 1997.
dc.identifier1023-3830
dc.identifierWOS:A1997WK96400007
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/81798
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/81798
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/81798
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1291562
dc.descriptionObjective: To assess involvement of nitric oxide (NO) in the increase in eicosanoid and interleukin-1 (IL-1) levels in the synovial fluid during antigen-induced arthritis (AIA) in rabbits treated with a competitive inhibitor of NO synthesis. Subjects: Thirteen New Zealand White rabbits were sensitized with 5 mg of methylated bovine serum albumin (mBSA). Arthritis was induced in the knee joint by injecting 0.5 ml of a sterile solution of mBSA (2 mg/ml) into the intra-articular cavity. Treatment: Prior to the induction of arthritis, the animals received N-Omega-Nitro-L-Arginine Methyl Ester (LNAME) or N-Omega-Nitro-D-Arginine Methyl Ester (DNAME) for 2 weeks, both at a dose of 20 mg/kg/day mixed with drinking water. Methods: Leukocyte efflux (total and differential white cell count), vascular permeability (Evans's blue method), synovial PMN cell infiltrate, and total nitrite (NO2.)/nitrate (NO3.) (HPLC), PGE(2), TxB(2), LTB(4) (radioimmunoassay), and IL-1 beta (ELISA) levels were quantified in the synovial fluid. Results: LNAME but not DNAME significantly suppressed leukocyte efflux and protein leakage into the articular cavity as well as synovial PMN cell infiltrate. Total NO2./NO3., PGE(2) and IL-1 beta levels were significantly reduced in the synovial fluid of LNAME treated animals. TxB(2) and LTB(4) were not affected by LNAME treatment. Conclusion: These data clearly show NO involvement in the IL-1-induced PGE(2) production in the synovial fluid of antigen-induced arthritis in rabbits.
dc.description46
dc.description2
dc.description72
dc.description77
dc.languageen
dc.publisherBirkhauser Verlag Ag
dc.publisherBasel
dc.publisherSuíça
dc.relationInflammation Research
dc.relationInflamm. Res.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectexperimental arthritis
dc.subjectnitric oxide
dc.subjecteicosanoids
dc.subjectinterleukin-1
dc.subjectMonomethyl-l-arginine
dc.subjectSmooth-muscle Cells
dc.subjectAdjuvant Arthritis
dc.subjectCyclooxygenase
dc.subjectActivation
dc.subjectE(2)
dc.subjectChondrocytes
dc.subjectInflammation
dc.subjectChemotaxis
dc.subjectCytokines
dc.titleNitric oxide synthase inhibitor influences prostaglandin and interleukin-1 production in experimental arthritic joints
dc.typeArtículos de revistas


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