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dc.creatorGoldstein Raij, Jorge-
dc.creatorCarden, Tomas Roberto-
dc.creatorPerez, María J.-
dc.creatorTaira, Carlos Alberto-
dc.creatorHöcht, Christian-
dc.creatorGironacci, Mariela Mercedes-
dc.date2018-06-05T21:51:18Z-
dc.date2018-06-05T21:51:18Z-
dc.date2016-12-
dc.date2018-06-05T20:11:35Z-
dc.date.accessioned2019-04-29T15:34:56Z-
dc.date.available2019-04-29T15:34:56Z-
dc.date.issued2018-06-05T21:51:18Z-
dc.date.issued2018-06-05T21:51:18Z-
dc.date.issued2016-12-
dc.date.issued2018-06-05T20:11:35Z-
dc.identifierGoldstein Raij, Jorge; Carden, Tomas Roberto; Perez, María J.; Taira, Carlos Alberto; Höcht, Christian; et al.; Angiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coli; American Physiological Society; American Journal Of Physiology-regulatory, Integrative And Comparative Physiology; 311; 6; 12-2016; 1173-1185-
dc.identifier0363-6119-
dc.identifierhttp://hdl.handle.net/11336/47423-
dc.identifierCONICET Digital-
dc.identifierCONICET-
dc.identifier.urihttp://rodna.bn.gov.ar:8080/jspui/handle/bnmm/297109-
dc.descriptionShiga toxin 2 (Stx2)-producing enterohemorrhagic induced brain damage. Since a cerebroprotective action was reported for angiotensin (Ang)-(1–7), our aim was to investigate whether Ang-(1–7) protects from brain damage induced by Stx2-producing enterohemorrhagic Escherichia coli. The anterior hypothalamic area of adult male Wistar rats was injected with saline solution or Stx2 or Stx2 plus Ang-(1–7) or Stx2 plus Ang-(1–7) plus A779. Rats received a single injection of Stx2 at the beginning of the experiment, and Ang-(1–7), A779, or saline was administered daily in a single injection for 8 days. Cellular ultrastructural changes were analyzed by transmission electron microscopy. Stx2 induced neurodegeneration, axonal demyelination, alterations in synapse, and oligodendrocyte and astrocyte damage, accompanied by edema. Ang-(1–7) prevented neuronal damage triggered by the toxin in 55.6 ± 9.5% of the neurons and the Stx2-induced synapse dysfunction was reversed. In addition, Ang-(1–7) blocked Stx2-induced demyelination in 92 ± 4% of the axons. Oligodendrocyte damage caused by Stx2 was prevented by Ang-(1–7) but astrocytes were only partially protected by the peptide (38 ± 5% of astrocytes were preserved). Ang-(1–7) treatment resulted in 50% reduction in the number of activated microglial cells induced by Stx2, suggesting an anti-inflammatory action. All these beneficial effects elicited by Ang-(1–7) were blocked by the Mas receptor antagonist and thus it was concluded that Ang-(1–7) protects mainly neurons and oligodendrocytes, and partially astrocytes, in the central nervous system through Mas receptor stimulation.-
dc.descriptionFil: Goldstein Raij, Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina-
dc.descriptionFil: Carden, Tomas Roberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina-
dc.descriptionFil: Perez, María J.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina-
dc.descriptionFil: Taira, Carlos Alberto. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina-
dc.descriptionFil: Höcht, Christian. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina-
dc.descriptionFil: Gironacci, Mariela Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina-
dc.formatapplication/pdf-
dc.formatapplication/zip-
dc.formatapplication/pdf-
dc.languageeng-
dc.publisherAmerican Physiological Society-
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1152/ajpregu.00467.2015-
dc.relationinfo:eu-repo/semantics/altIdentifier/url/https://www.physiology.org/doi/10.1152/ajpregu.00467.2015-
dc.rightsinfo:eu-repo/semantics/restrictedAccess-
dc.rightshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/-
dc.sourcereponame:CONICET Digital (CONICET)-
dc.sourceinstname:Consejo Nacional de Investigaciones Científicas y Técnicas-
dc.sourceinstacron:CONICET-
dc.subjectANGIOTENSIN-(1-7)-
dc.subjectMAS RECEPTOR-
dc.subjectNEURON-
dc.subjectOLIGODENDROCYTE-
dc.subjectASTROCYTE-
dc.subjectSalud Ocupacional-
dc.subjectCiencias de la Salud-
dc.subjectCIENCIAS MÉDICAS Y DE LA SALUD-
dc.titleAngiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coli-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:eu-repo/semantics/publishedVersion-
dc.typeinfo:ar-repo/semantics/articulo-
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