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dc.contributor.authorBrigatte, Patricia
dc.contributor.authorFaiad, Odair Jorge
dc.contributor.authorFerreira Nocelli, Roberta Cornelio
dc.contributor.authorLandgraf, Richardt G. [UNIFESP]
dc.contributor.authorPalma, Mario Sergio
dc.contributor.authorCury, Yara
dc.contributor.authorCuri, Rui
dc.contributor.authorSampaio, Sandra Coccuzzo
dc.date.accessioned2019-01-21T10:30:00Z
dc.date.available2019-01-21T10:30:00Z
dc.date.issued2016
dc.identifierhttp://dx.doi.org/10.1155/2016/2457532
dc.identifier.citationMediators Of Inflammation. London, 2016.
dc.identifier.issn0962-9351
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/49524
dc.description.abstractWe investigated the effects of Crotoxin (CTX), the main toxin of South American rattlesnake (Crotalus durissus terrificus) venom, on Walker 256 tumor growth, the pain symptoms associated (hyperalgesia and allodynia), and participation of endogenous lipoxin A(4). Treatment with CTX (s.c.), daily, for 5 days reduced tumor growth at the 5th day after injection of Walker 256 carcinoma cells into the plantar surface of adult rat hind paw. This observation was associated with inhibition of new blood vessel formation and decrease in blood vessel diameter. The treatment with CTX raised plasma concentrations of lipoxin A 4 and its natural analogue 15-epi-LXA(4) 4, an effect mediated by formyl peptide receptors (FPRs). In fact, the treatment with Boc-2, an inhibitor of FPRs, abolished the increase in plasma levels of these mediators triggered by CTX. The blockage of these receptors also abolished the inhibitory action of CTX on tumor growth and blood vessel formation and the decrease in blood vessel diameter. Together, the results herein presented demonstrate that CTX increases plasma concentrations of lipoxin A 4 and 15-epi-LXA 4, which might inhibit both tumor growth and formation of new vessels via FPRs.en
dc.description.sponsorshipCoordenacao de Aperfeicoamento de Pessoal de Nivel Superior (fellowship-CAPES)
dc.description.sponsorshipPAP (fellowship-Secretaria da Saude do Estado de Sao Paulo)
dc.description.sponsorshipFAPESP [07/52447-8]
dc.description.sponsorshipGuggenheim Foundation
dc.language.isoeng
dc.publisherHindawi ltd
dc.relation.ispartofMediators Of Inflammation
dc.rightsAcesso aberto
dc.subjectCrotalus-Durissus-Terrificusen
dc.subjectAspirin-Triggered Lipoxinsen
dc.subjectArachidonic-Aciden
dc.subjectSnake-Venomen
dc.subjectAntiangiogenic Therapyen
dc.subjectCell-Proliferationen
dc.subjectLipid Mediatorsen
dc.subjectAnalog Suppressen
dc.subjectCobra Venomen
dc.subjectCancer Painen
dc.titleWalker 256 tumor growth suppression by crotoxin involves formyl peptide receptors and lipoxin a(4)en
dc.typeArtigo
dc.description.affiliationSpecial Laboratory of Pain and Signaling, Butantan Institute, Avenida Vital Brazil 1500, 05503-900 São Paulo, SP, Brazil
dc.description.affiliationCEIS/Department of Biology, Institute of Biosciences of Rio Claro, São Paulo State University (UNESP), Rio Claro, SP, Brazil
dc.description.affiliationLaboratory of Pathophysiology, Butantan Institute, Avenida Vital Brazil 1500, 05503-900 São Paulo, SP, Brazil
dc.description.affiliationDepartment of Natural Sciences, Mathematics and Education, Agricultural Sciences Center, Federal University of São Carlos, Rodovia Anhanguera Km 174, 13600-970 Araras, SP, Brazil
dc.description.affiliationLaboratory of Inflammation and Vascular Pharmacology, Federal University of São Paulo, Rua São Nicolau 210, 09913-030 Diadema, SP, Brazil
dc.description.affiliationDepartment of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, Avenida Professor Lineu Prestes 1524, 05508-900 São Paulo, SP, Brazil
dc.description.affiliationDepartment of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, Avenida Professor Lineu Prestes 1524, 05508-900 São Paulo, SP, Brazil
dc.description.affiliationUnifespLaboratory of Inflammation and Vascular Pharmacology, Federal University of São Paulo, Rua São Nicolau 210, 09913-030 Diadema, SP, Brazil
dc.description.sponsorshipIDFAPESP: 07/52447-8
dc.identifier.fileWOS000374851200001.pdf
dc.identifier.doi10.1155/2016/2457532
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000374851200001


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