Endocannabinoids mediate hyposalivation induced by inflammogens in the submandibular glands and hypothalamus

Autores
Prestifilippo, Juan Pablo; Medina, Vanina Araceli; Mohn, Claudia Ester; Rodriguez, P. A.; Elverdin, Juan Carlos; Fernández Solari, Jose Javier
Año de publicación
2013
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Objective: The aim of this study was to investigate the factors that could participate on salivary glands hypofunction during inflammation and the participation of endocannabinoids in hyposalivation induced by the presence of inflammogens in the submandibular gland (SMG) or in the brain. Design: Salivary secretion was assessed in the presence of inflammogens and/or the cannabinoid receptor antagonist AM251 in the SMG or in the brain of rats. At the end of the experiments, some systemic and glandular inflammatory markers were measured and histopathological analysis was performed. Results: The inhibitory effect observed 1 h after lipopolysaccharide (LPS, 50 μg/50 μl) injection into the SMG (ig) was completely prevented by the injection of AM251 (5 μg/50 μl) by the same route (P < 0.05). The LPS (ig)-induced increase in PGE2 content was not altered by AM251 (ig), while the glandular production of TNFa induced by the endotoxin (P < 0.001) was partially blocked by it. Also, LPS injection produced no significant changes in the wet weight of the SMG neither damage to lipid membranes of its cells, nor significant microscopic changes in them, after hispopathological analysis, compared to controls. Finally, TNFα (100 ng/5 μl) injected intracerebro-ventricularly (icv) inhibited methacholine-induced salivary secretion evaluated 30 min after (P < 0.01), but the previous injection of AM251 (500 ng/5 μl, icv) prevented completely that effect. Conclusion: We conclude that endocannabinoids mediate the hyposialia induced by inflammogens in the SMG and in the brain. The hypofunction would be due to changes on signalling pathway produced by inflammatory compounds since anatomical changes were not observed. © 2013 Elsevier Ltd. All rights reserved.
Fil: Prestifilippo, Juan Pablo. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Fisiología; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina
Fil: Medina, Vanina Araceli. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Fisicomatemática. Cátedra de Física; Argentina
Fil: Mohn, Claudia Ester. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Fisiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
Fil: Rodriguez, P. A.. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - La Plata. Unidad de Administración Territorial; Argentina. Universidad de Buenos Aires. Facultad de Odontología; Argentina
Fil: Elverdin, Juan Carlos. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Fisiología; Argentina
Fil: Fernández Solari, Jose Javier. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Fisiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
Materia
ENDOCANNABINOID SYSTEM
LIPOPOLYSACCHARIDE
PROSTAGLANDIN E2
SALIVA
TUMOUR NECROSIS FACTOR ALPHA
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/1906
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/1906
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Endocannabinoids mediate hyposalivation induced by inflammogens in the submandibular glands and hypothalamusPrestifilippo, Juan PabloMedina, Vanina AraceliMohn, Claudia EsterRodriguez, P. A.Elverdin, Juan CarlosFernández Solari, Jose JavierENDOCANNABINOID SYSTEMLIPOPOLYSACCHARIDEPROSTAGLANDIN E2SALIVATUMOUR NECROSIS FACTOR ALPHAhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3https://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3Objective: The aim of this study was to investigate the factors that could participate on salivary glands hypofunction during inflammation and the participation of endocannabinoids in hyposalivation induced by the presence of inflammogens in the submandibular gland (SMG) or in the brain. Design: Salivary secretion was assessed in the presence of inflammogens and/or the cannabinoid receptor antagonist AM251 in the SMG or in the brain of rats. At the end of the experiments, some systemic and glandular inflammatory markers were measured and histopathological analysis was performed. Results: The inhibitory effect observed 1 h after lipopolysaccharide (LPS, 50 μg/50 μl) injection into the SMG (ig) was completely prevented by the injection of AM251 (5 μg/50 μl) by the same route (P < 0.05). The LPS (ig)-induced increase in PGE2 content was not altered by AM251 (ig), while the glandular production of TNFa induced by the endotoxin (P < 0.001) was partially blocked by it. Also, LPS injection produced no significant changes in the wet weight of the SMG neither damage to lipid membranes of its cells, nor significant microscopic changes in them, after hispopathological analysis, compared to controls. Finally, TNFα (100 ng/5 μl) injected intracerebro-ventricularly (icv) inhibited methacholine-induced salivary secretion evaluated 30 min after (P < 0.01), but the previous injection of AM251 (500 ng/5 μl, icv) prevented completely that effect. Conclusion: We conclude that endocannabinoids mediate the hyposialia induced by inflammogens in the SMG and in the brain. The hypofunction would be due to changes on signalling pathway produced by inflammatory compounds since anatomical changes were not observed. © 2013 Elsevier Ltd. All rights reserved.Fil: Prestifilippo, Juan Pablo. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Fisiología; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; ArgentinaFil: Medina, Vanina Araceli. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Fisicomatemática. Cátedra de Física; ArgentinaFil: Mohn, Claudia Ester. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Fisiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; ArgentinaFil: Rodriguez, P. A.. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - La Plata. Unidad de Administración Territorial; Argentina. Universidad de Buenos Aires. Facultad de Odontología; ArgentinaFil: Elverdin, Juan Carlos. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Fisiología; ArgentinaFil: Fernández Solari, Jose Javier. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Fisiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; ArgentinaPergamon-Elsevier Science Ltd2013-09info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/1906Prestifilippo, Juan Pablo; Medina, Vanina Araceli; Mohn, Claudia Ester; Rodriguez, P. A.; Elverdin, Juan Carlos; et al.; Endocannabinoids mediate hyposalivation induced by inflammogens in the submandibular glands and hypothalamus; Pergamon-Elsevier Science Ltd; Archives of Oral Biology; 58; 9; 9-2013; 1251-12590003-9969enginfo:eu-repo/semantics/reference/url/info:eu-repo/semantics/reference es info:eu-repo/semantics/reference/pmid/23684250info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0003996913001179info:eu-repo/semantics/altIdentifier/url/http://www.odon.uba.ar/uacad/fisiologia/docs/nuevos/arch_oral_biol_2013.pdfinfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.archoralbio.2013.04.003info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:08:13Zoai:ri.conicet.gov.ar:11336/1906instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:08:13.651CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Endocannabinoids mediate hyposalivation induced by inflammogens in the submandibular glands and hypothalamus
title Endocannabinoids mediate hyposalivation induced by inflammogens in the submandibular glands and hypothalamus
spellingShingle Endocannabinoids mediate hyposalivation induced by inflammogens in the submandibular glands and hypothalamus
Prestifilippo, Juan Pablo
ENDOCANNABINOID SYSTEM
LIPOPOLYSACCHARIDE
PROSTAGLANDIN E2
SALIVA
TUMOUR NECROSIS FACTOR ALPHA
title_short Endocannabinoids mediate hyposalivation induced by inflammogens in the submandibular glands and hypothalamus
title_full Endocannabinoids mediate hyposalivation induced by inflammogens in the submandibular glands and hypothalamus
title_fullStr Endocannabinoids mediate hyposalivation induced by inflammogens in the submandibular glands and hypothalamus
title_full_unstemmed Endocannabinoids mediate hyposalivation induced by inflammogens in the submandibular glands and hypothalamus
title_sort Endocannabinoids mediate hyposalivation induced by inflammogens in the submandibular glands and hypothalamus
dc.creator.none.fl_str_mv Prestifilippo, Juan Pablo
Medina, Vanina Araceli
Mohn, Claudia Ester
Rodriguez, P. A.
Elverdin, Juan Carlos
Fernández Solari, Jose Javier
author Prestifilippo, Juan Pablo
author_facet Prestifilippo, Juan Pablo
Medina, Vanina Araceli
Mohn, Claudia Ester
Rodriguez, P. A.
Elverdin, Juan Carlos
Fernández Solari, Jose Javier
author_role author
author2 Medina, Vanina Araceli
Mohn, Claudia Ester
Rodriguez, P. A.
Elverdin, Juan Carlos
Fernández Solari, Jose Javier
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv ENDOCANNABINOID SYSTEM
LIPOPOLYSACCHARIDE
PROSTAGLANDIN E2
SALIVA
TUMOUR NECROSIS FACTOR ALPHA
topic ENDOCANNABINOID SYSTEM
LIPOPOLYSACCHARIDE
PROSTAGLANDIN E2
SALIVA
TUMOUR NECROSIS FACTOR ALPHA
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Objective: The aim of this study was to investigate the factors that could participate on salivary glands hypofunction during inflammation and the participation of endocannabinoids in hyposalivation induced by the presence of inflammogens in the submandibular gland (SMG) or in the brain. Design: Salivary secretion was assessed in the presence of inflammogens and/or the cannabinoid receptor antagonist AM251 in the SMG or in the brain of rats. At the end of the experiments, some systemic and glandular inflammatory markers were measured and histopathological analysis was performed. Results: The inhibitory effect observed 1 h after lipopolysaccharide (LPS, 50 μg/50 μl) injection into the SMG (ig) was completely prevented by the injection of AM251 (5 μg/50 μl) by the same route (P < 0.05). The LPS (ig)-induced increase in PGE2 content was not altered by AM251 (ig), while the glandular production of TNFa induced by the endotoxin (P < 0.001) was partially blocked by it. Also, LPS injection produced no significant changes in the wet weight of the SMG neither damage to lipid membranes of its cells, nor significant microscopic changes in them, after hispopathological analysis, compared to controls. Finally, TNFα (100 ng/5 μl) injected intracerebro-ventricularly (icv) inhibited methacholine-induced salivary secretion evaluated 30 min after (P < 0.01), but the previous injection of AM251 (500 ng/5 μl, icv) prevented completely that effect. Conclusion: We conclude that endocannabinoids mediate the hyposialia induced by inflammogens in the SMG and in the brain. The hypofunction would be due to changes on signalling pathway produced by inflammatory compounds since anatomical changes were not observed. © 2013 Elsevier Ltd. All rights reserved.
Fil: Prestifilippo, Juan Pablo. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Fisiología; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina
Fil: Medina, Vanina Araceli. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Fisicomatemática. Cátedra de Física; Argentina
Fil: Mohn, Claudia Ester. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Fisiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
Fil: Rodriguez, P. A.. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - La Plata. Unidad de Administración Territorial; Argentina. Universidad de Buenos Aires. Facultad de Odontología; Argentina
Fil: Elverdin, Juan Carlos. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Fisiología; Argentina
Fil: Fernández Solari, Jose Javier. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Fisiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
description Objective: The aim of this study was to investigate the factors that could participate on salivary glands hypofunction during inflammation and the participation of endocannabinoids in hyposalivation induced by the presence of inflammogens in the submandibular gland (SMG) or in the brain. Design: Salivary secretion was assessed in the presence of inflammogens and/or the cannabinoid receptor antagonist AM251 in the SMG or in the brain of rats. At the end of the experiments, some systemic and glandular inflammatory markers were measured and histopathological analysis was performed. Results: The inhibitory effect observed 1 h after lipopolysaccharide (LPS, 50 μg/50 μl) injection into the SMG (ig) was completely prevented by the injection of AM251 (5 μg/50 μl) by the same route (P < 0.05). The LPS (ig)-induced increase in PGE2 content was not altered by AM251 (ig), while the glandular production of TNFa induced by the endotoxin (P < 0.001) was partially blocked by it. Also, LPS injection produced no significant changes in the wet weight of the SMG neither damage to lipid membranes of its cells, nor significant microscopic changes in them, after hispopathological analysis, compared to controls. Finally, TNFα (100 ng/5 μl) injected intracerebro-ventricularly (icv) inhibited methacholine-induced salivary secretion evaluated 30 min after (P < 0.01), but the previous injection of AM251 (500 ng/5 μl, icv) prevented completely that effect. Conclusion: We conclude that endocannabinoids mediate the hyposialia induced by inflammogens in the SMG and in the brain. The hypofunction would be due to changes on signalling pathway produced by inflammatory compounds since anatomical changes were not observed. © 2013 Elsevier Ltd. All rights reserved.
publishDate 2013
dc.date.none.fl_str_mv 2013-09
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/1906
Prestifilippo, Juan Pablo; Medina, Vanina Araceli; Mohn, Claudia Ester; Rodriguez, P. A.; Elverdin, Juan Carlos; et al.; Endocannabinoids mediate hyposalivation induced by inflammogens in the submandibular glands and hypothalamus; Pergamon-Elsevier Science Ltd; Archives of Oral Biology; 58; 9; 9-2013; 1251-1259
0003-9969
url http://hdl.handle.net/11336/1906
identifier_str_mv Prestifilippo, Juan Pablo; Medina, Vanina Araceli; Mohn, Claudia Ester; Rodriguez, P. A.; Elverdin, Juan Carlos; et al.; Endocannabinoids mediate hyposalivation induced by inflammogens in the submandibular glands and hypothalamus; Pergamon-Elsevier Science Ltd; Archives of Oral Biology; 58; 9; 9-2013; 1251-1259
0003-9969
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/reference/url/info:eu-repo/semantics/reference es info:eu-repo/semantics/reference/pmid/23684250
info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0003996913001179
info:eu-repo/semantics/altIdentifier/url/http://www.odon.uba.ar/uacad/fisiologia/docs/nuevos/arch_oral_biol_2013.pdf
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.archoralbio.2013.04.003
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Pergamon-Elsevier Science Ltd
publisher.none.fl_str_mv Pergamon-Elsevier Science Ltd
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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