Diacerein improves left ventricular remodeling and cardiac function by reducing the inflammatory response after myocardial infarction.

The inflammatory response has been implicated in the pathogenesis of left ventricular (LV) remodeling after myocardial infarction (MI). An anthraquinone compound with anti-inflammatory properties, diacerein inhibits the synthesis and activity of pro-inflammatory cytokines, such as tumor necrosis fac...

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Main Authors: Anali Galluce Torina, Karla Reichert, Fany Lima, Karlos Alexandre de Souza Vilarinho, Pedro Paulo Martins de Oliveira, Helison Rafael Pereira do Carmo, Daniela Diógenes de Carvalho, Mário José Abdalla Saad, Andrei Carvalho Sposito, Orlando Petrucci
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2015-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4376692?pdf=render
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author Anali Galluce Torina
Karla Reichert
Fany Lima
Karlos Alexandre de Souza Vilarinho
Pedro Paulo Martins de Oliveira
Helison Rafael Pereira do Carmo
Daniela Diógenes de Carvalho
Mário José Abdalla Saad
Andrei Carvalho Sposito
Orlando Petrucci
author_facet Anali Galluce Torina
Karla Reichert
Fany Lima
Karlos Alexandre de Souza Vilarinho
Pedro Paulo Martins de Oliveira
Helison Rafael Pereira do Carmo
Daniela Diógenes de Carvalho
Mário José Abdalla Saad
Andrei Carvalho Sposito
Orlando Petrucci
author_sort Anali Galluce Torina
collection DOAJ
description The inflammatory response has been implicated in the pathogenesis of left ventricular (LV) remodeling after myocardial infarction (MI). An anthraquinone compound with anti-inflammatory properties, diacerein inhibits the synthesis and activity of pro-inflammatory cytokines, such as tumor necrosis factor and interleukins 1 and 6. The purpose of this study was to investigate the effects of diacerein on ventricular remodeling in vivo.Ligation of the left anterior descending artery was used to induce MI in an experimental rat model. Rats were divided into two groups: a control group that received saline solution (n = 16) and a group that received diacerein (80 mg/kg) daily (n = 10). After 4 weeks, the LV volume, cellular signaling, caspase 3 activity, and nuclear factor kappa B (NF-κB) transcription were compared between the two groups. After 4 weeks, end-diastolic and end-systolic LV volumes were reduced in the treatment group compared to the control group (p < .01 and p < .01, respectively). Compared to control rats, diacerein-treated rats exhibited less fibrosis in the LV (14.65%± 7.27% vs. 22.57%± 8.94%; p < .01), lower levels of caspase-3 activity, and lower levels of NF-κB p65 transcription.Treatment with diacerein once a day for 4 weeks after MI improved ventricular remodeling by promoting lower end-systolic and end-diastolic LV volumes. Diacerein also reduced fibrosis in the LV. These effects might be associated with partial blockage of the NF-κB pathway.
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spelling doaj.art-bdcd8a2cfbe74ca88c86c4f9671dd22c2022-12-21T19:10:16ZengPublic Library of Science (PLoS)PLoS ONE1932-62032015-01-01103e012184210.1371/journal.pone.0121842Diacerein improves left ventricular remodeling and cardiac function by reducing the inflammatory response after myocardial infarction.Anali Galluce TorinaKarla ReichertFany LimaKarlos Alexandre de Souza VilarinhoPedro Paulo Martins de OliveiraHelison Rafael Pereira do CarmoDaniela Diógenes de CarvalhoMário José Abdalla SaadAndrei Carvalho SpositoOrlando PetrucciThe inflammatory response has been implicated in the pathogenesis of left ventricular (LV) remodeling after myocardial infarction (MI). An anthraquinone compound with anti-inflammatory properties, diacerein inhibits the synthesis and activity of pro-inflammatory cytokines, such as tumor necrosis factor and interleukins 1 and 6. The purpose of this study was to investigate the effects of diacerein on ventricular remodeling in vivo.Ligation of the left anterior descending artery was used to induce MI in an experimental rat model. Rats were divided into two groups: a control group that received saline solution (n = 16) and a group that received diacerein (80 mg/kg) daily (n = 10). After 4 weeks, the LV volume, cellular signaling, caspase 3 activity, and nuclear factor kappa B (NF-κB) transcription were compared between the two groups. After 4 weeks, end-diastolic and end-systolic LV volumes were reduced in the treatment group compared to the control group (p < .01 and p < .01, respectively). Compared to control rats, diacerein-treated rats exhibited less fibrosis in the LV (14.65%± 7.27% vs. 22.57%± 8.94%; p < .01), lower levels of caspase-3 activity, and lower levels of NF-κB p65 transcription.Treatment with diacerein once a day for 4 weeks after MI improved ventricular remodeling by promoting lower end-systolic and end-diastolic LV volumes. Diacerein also reduced fibrosis in the LV. These effects might be associated with partial blockage of the NF-κB pathway.http://europepmc.org/articles/PMC4376692?pdf=render
spellingShingle Anali Galluce Torina
Karla Reichert
Fany Lima
Karlos Alexandre de Souza Vilarinho
Pedro Paulo Martins de Oliveira
Helison Rafael Pereira do Carmo
Daniela Diógenes de Carvalho
Mário José Abdalla Saad
Andrei Carvalho Sposito
Orlando Petrucci
Diacerein improves left ventricular remodeling and cardiac function by reducing the inflammatory response after myocardial infarction.
PLoS ONE
title Diacerein improves left ventricular remodeling and cardiac function by reducing the inflammatory response after myocardial infarction.
title_full Diacerein improves left ventricular remodeling and cardiac function by reducing the inflammatory response after myocardial infarction.
title_fullStr Diacerein improves left ventricular remodeling and cardiac function by reducing the inflammatory response after myocardial infarction.
title_full_unstemmed Diacerein improves left ventricular remodeling and cardiac function by reducing the inflammatory response after myocardial infarction.
title_short Diacerein improves left ventricular remodeling and cardiac function by reducing the inflammatory response after myocardial infarction.
title_sort diacerein improves left ventricular remodeling and cardiac function by reducing the inflammatory response after myocardial infarction
url http://europepmc.org/articles/PMC4376692?pdf=render
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