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Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure

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-prolife...

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Autores principales: Minicucci, Marcos, Oliveira, Fernando, Santos, Priscila, Polegato, Bertha, Roscani, Meliza, Fernandes, Ana Angelica, Lustosa, Beatriz, Paiva, Sergio, Zornoff, Leonardo, Azevedo, Paula
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Sociedade Brasileira de Cardiologia - SBC 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4914004/
https://www.ncbi.nlm.nih.gov/pubmed/27096523
http://dx.doi.org/10.5935/abc.20160057
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author Minicucci, Marcos
Oliveira, Fernando
Santos, Priscila
Polegato, Bertha
Roscani, Meliza
Fernandes, Ana Angelica
Lustosa, Beatriz
Paiva, Sergio
Zornoff, Leonardo
Azevedo, Paula
author_facet Minicucci, Marcos
Oliveira, Fernando
Santos, Priscila
Polegato, Bertha
Roscani, Meliza
Fernandes, Ana Angelica
Lustosa, Beatriz
Paiva, Sergio
Zornoff, Leonardo
Azevedo, Paula
author_sort Minicucci, Marcos
collection PubMed
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.
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spelling pubmed-49140042016-06-21 Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure Minicucci, Marcos Oliveira, Fernando Santos, Priscila Polegato, Bertha Roscani, Meliza Fernandes, Ana Angelica Lustosa, Beatriz Paiva, Sergio Zornoff, Leonardo Azevedo, Paula Arq Bras Cardiol Original Articles 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. Sociedade Brasileira de Cardiologia - SBC 2016-05 /pmc/articles/PMC4914004/ /pubmed/27096523 http://dx.doi.org/10.5935/abc.20160057 Text en http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Minicucci, Marcos
Oliveira, Fernando
Santos, Priscila
Polegato, Bertha
Roscani, Meliza
Fernandes, Ana Angelica
Lustosa, Beatriz
Paiva, Sergio
Zornoff, Leonardo
Azevedo, Paula
Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure
title 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_short Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure
title_sort pentoxifylline attenuates cardiac remodeling induced by tobacco smoke exposure
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4914004/
https://www.ncbi.nlm.nih.gov/pubmed/27096523
http://dx.doi.org/10.5935/abc.20160057
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