Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure
Autor(a) principal: | |
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Data de Publicação: | 2016 |
Outros Autores: | , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.5935/abc.20160057 http://hdl.handle.net/11449/165222 |
Resumo: | Background: Tobacco smoke exposure is an important risk factor for cardiac remodeling. Under this condition, inflammation, oxidative stress, energy metabolism abnormalities, apoptosis, and hypertrophy are present. Pentoxifylline has anti-inflammatory, anti-apoptotic, anti-thrombotic and anti-proliferative properties. Objective: The present study tested the hypothesis that pentoxifylline would attenuate cardiac remodeling induced by smoking. Methods: Wistar rats were distributed in four groups: Control (C), Pentoxifylline (PX), Tobacco Smoke (TS), and PX-TS. After two months, echocardiography, invasive blood pressure measurement, biochemical, and histological studies were performed. The groups were compared by two-way ANOVA with a significance level of 5%. Results: TS increased left atrium diameter and area, which was attenuated by PX. In the isolated heart study, TS lowered the positive derivate (+dp/dt), and this was attenuated by PX. The antioxidants enzyme superoxide dismutase and glutathione peroxidase were decreased in the TS group; PX recovered these activities. TS increased lactate dehydrogenase (LDH) and decreased 3-hydroxyacyl Coenzyme A dehydrogenases (OH-DHA) and citrate synthase (CS). PX attenuated LDH, 3-OH-DHA and CS alterations in TS-PX group. TS increased IL-10, ICAM-1, and caspase-3. PX did not influence these variables. Conclusion: TS induced cardiac remodeling, associated with increased inflammation, oxidative stress, apoptosis, and changed energy metabolism. PX attenuated cardiac remodeling by reducing oxidative stress and improving cardiac bioenergetics, but did not act upon cardiac cytokines and apoptosis. |
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Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke ExposureTobacco Smoke PollutionVentricular RemodelingPentoxifyllineOxidative StressCardiomyopathiesBackground: Tobacco smoke exposure is an important risk factor for cardiac remodeling. Under this condition, inflammation, oxidative stress, energy metabolism abnormalities, apoptosis, and hypertrophy are present. Pentoxifylline has anti-inflammatory, anti-apoptotic, anti-thrombotic and anti-proliferative properties. Objective: The present study tested the hypothesis that pentoxifylline would attenuate cardiac remodeling induced by smoking. Methods: Wistar rats were distributed in four groups: Control (C), Pentoxifylline (PX), Tobacco Smoke (TS), and PX-TS. After two months, echocardiography, invasive blood pressure measurement, biochemical, and histological studies were performed. The groups were compared by two-way ANOVA with a significance level of 5%. Results: TS increased left atrium diameter and area, which was attenuated by PX. In the isolated heart study, TS lowered the positive derivate (+dp/dt), and this was attenuated by PX. The antioxidants enzyme superoxide dismutase and glutathione peroxidase were decreased in the TS group; PX recovered these activities. TS increased lactate dehydrogenase (LDH) and decreased 3-hydroxyacyl Coenzyme A dehydrogenases (OH-DHA) and citrate synthase (CS). PX attenuated LDH, 3-OH-DHA and CS alterations in TS-PX group. TS increased IL-10, ICAM-1, and caspase-3. PX did not influence these variables. Conclusion: TS induced cardiac remodeling, associated with increased inflammation, oxidative stress, apoptosis, and changed energy metabolism. PX attenuated cardiac remodeling by reducing oxidative stress and improving cardiac bioenergetics, but did not act upon cardiac cytokines and apoptosis.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Univ Estadual Paulista, Fac Med Botucatu, Sao Paulo, SP, BrazilUniv Estadual Paulista, Fac Med Botucatu, Sao Paulo, SP, BrazilArquivos Brasileiros CardiologiaUniversidade Estadual Paulista (Unesp)Minicucci, Marcos [UNESP]Oliveira, Fernando [UNESP]Santos, Priscila [UNESP]Polegato, Bertha [UNESP]Roscani, Meliza [UNESP]Fernandes, Ana Angelica [UNESP]Lustosa, Beatriz [UNESP]Paiva, Sergio [UNESP]Zornoff, Leonardo [UNESP]Azevedo, Paula [UNESP]2018-11-27T16:55:47Z2018-11-27T16:55:47Z2016-05-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article396-403application/pdfhttp://dx.doi.org/10.5935/abc.20160057Arquivos Brasileiros De Cardiologia. Rio De Janeiro: Arquivos Brasileiros Cardiologia, v. 106, n. 5, p. 396-403, 2016.0066-782Xhttp://hdl.handle.net/11449/16522210.5935/abc.20160057S0066-782X2016000500396WOS:000379040700007S0066-782X2016000500396.pdfWeb of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengArquivos Brasileiros De Cardiologiainfo:eu-repo/semantics/openAccess2024-08-14T17:23:44Zoai:repositorio.unesp.br:11449/165222Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-14T17:23:44Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure |
title |
Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure |
spellingShingle |
Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure Minicucci, Marcos [UNESP] Tobacco Smoke Pollution Ventricular Remodeling Pentoxifylline Oxidative Stress Cardiomyopathies |
title_short |
Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure |
title_full |
Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure |
title_fullStr |
Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure |
title_full_unstemmed |
Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure |
title_sort |
Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure |
author |
Minicucci, Marcos [UNESP] |
author_facet |
Minicucci, Marcos [UNESP] Oliveira, Fernando [UNESP] Santos, Priscila [UNESP] Polegato, Bertha [UNESP] Roscani, Meliza [UNESP] Fernandes, Ana Angelica [UNESP] Lustosa, Beatriz [UNESP] Paiva, Sergio [UNESP] Zornoff, Leonardo [UNESP] Azevedo, Paula [UNESP] |
author_role |
author |
author2 |
Oliveira, Fernando [UNESP] Santos, Priscila [UNESP] Polegato, Bertha [UNESP] Roscani, Meliza [UNESP] Fernandes, Ana Angelica [UNESP] Lustosa, Beatriz [UNESP] Paiva, Sergio [UNESP] Zornoff, Leonardo [UNESP] Azevedo, Paula [UNESP] |
author2_role |
author author author author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Estadual Paulista (Unesp) |
dc.contributor.author.fl_str_mv |
Minicucci, Marcos [UNESP] Oliveira, Fernando [UNESP] Santos, Priscila [UNESP] Polegato, Bertha [UNESP] Roscani, Meliza [UNESP] Fernandes, Ana Angelica [UNESP] Lustosa, Beatriz [UNESP] Paiva, Sergio [UNESP] Zornoff, Leonardo [UNESP] Azevedo, Paula [UNESP] |
dc.subject.por.fl_str_mv |
Tobacco Smoke Pollution Ventricular Remodeling Pentoxifylline Oxidative Stress Cardiomyopathies |
topic |
Tobacco Smoke Pollution Ventricular Remodeling Pentoxifylline Oxidative Stress Cardiomyopathies |
description |
Background: Tobacco smoke exposure is an important risk factor for cardiac remodeling. Under this condition, inflammation, oxidative stress, energy metabolism abnormalities, apoptosis, and hypertrophy are present. Pentoxifylline has anti-inflammatory, anti-apoptotic, anti-thrombotic and anti-proliferative properties. Objective: The present study tested the hypothesis that pentoxifylline would attenuate cardiac remodeling induced by smoking. Methods: Wistar rats were distributed in four groups: Control (C), Pentoxifylline (PX), Tobacco Smoke (TS), and PX-TS. After two months, echocardiography, invasive blood pressure measurement, biochemical, and histological studies were performed. The groups were compared by two-way ANOVA with a significance level of 5%. Results: TS increased left atrium diameter and area, which was attenuated by PX. In the isolated heart study, TS lowered the positive derivate (+dp/dt), and this was attenuated by PX. The antioxidants enzyme superoxide dismutase and glutathione peroxidase were decreased in the TS group; PX recovered these activities. TS increased lactate dehydrogenase (LDH) and decreased 3-hydroxyacyl Coenzyme A dehydrogenases (OH-DHA) and citrate synthase (CS). PX attenuated LDH, 3-OH-DHA and CS alterations in TS-PX group. TS increased IL-10, ICAM-1, and caspase-3. PX did not influence these variables. Conclusion: TS induced cardiac remodeling, associated with increased inflammation, oxidative stress, apoptosis, and changed energy metabolism. PX attenuated cardiac remodeling by reducing oxidative stress and improving cardiac bioenergetics, but did not act upon cardiac cytokines and apoptosis. |
publishDate |
2016 |
dc.date.none.fl_str_mv |
2016-05-01 2018-11-27T16:55:47Z 2018-11-27T16:55:47Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.5935/abc.20160057 Arquivos Brasileiros De Cardiologia. Rio De Janeiro: Arquivos Brasileiros Cardiologia, v. 106, n. 5, p. 396-403, 2016. 0066-782X http://hdl.handle.net/11449/165222 10.5935/abc.20160057 S0066-782X2016000500396 WOS:000379040700007 S0066-782X2016000500396.pdf |
url |
http://dx.doi.org/10.5935/abc.20160057 http://hdl.handle.net/11449/165222 |
identifier_str_mv |
Arquivos Brasileiros De Cardiologia. Rio De Janeiro: Arquivos Brasileiros Cardiologia, v. 106, n. 5, p. 396-403, 2016. 0066-782X 10.5935/abc.20160057 S0066-782X2016000500396 WOS:000379040700007 S0066-782X2016000500396.pdf |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Arquivos Brasileiros De Cardiologia |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
396-403 application/pdf |
dc.publisher.none.fl_str_mv |
Arquivos Brasileiros Cardiologia |
publisher.none.fl_str_mv |
Arquivos Brasileiros Cardiologia |
dc.source.none.fl_str_mv |
Web of Science reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
|
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1808128178157256704 |