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Lycopene Ameliorates Liver Inflammation and Redox Status in Mice Exposed to Long-Term Cigarette Smoke

Cigarette smoke (CS) is the major cause of preventable death worldwide, and it can also cause damage to extrapulmonary organs, such as the liver, mainly due the generation of reactive oxygen species (ROS). The liver is an essential organ for human survival since it is mainly responsible for the body...

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Autores principales: Rocha, Daniela Fonseca Abdo, Machado-Junior, Pedro Alves, Souza, Ana Beatriz Farias, Castro, Thalles de Freitas, Costa, Guilherme de Paula, Talvani, André, Bezerra, Frank Silva, Cangussú, Silvia Dantas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8639233/
https://www.ncbi.nlm.nih.gov/pubmed/34869769
http://dx.doi.org/10.1155/2021/7101313
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author Rocha, Daniela Fonseca Abdo
Machado-Junior, Pedro Alves
Souza, Ana Beatriz Farias
Castro, Thalles de Freitas
Costa, Guilherme de Paula
Talvani, André
Bezerra, Frank Silva
Cangussú, Silvia Dantas
author_facet Rocha, Daniela Fonseca Abdo
Machado-Junior, Pedro Alves
Souza, Ana Beatriz Farias
Castro, Thalles de Freitas
Costa, Guilherme de Paula
Talvani, André
Bezerra, Frank Silva
Cangussú, Silvia Dantas
author_sort Rocha, Daniela Fonseca Abdo
collection PubMed
description Cigarette smoke (CS) is the major cause of preventable death worldwide, and it can also cause damage to extrapulmonary organs, such as the liver, mainly due the generation of reactive oxygen species (ROS). The liver is an essential organ for human survival since it is mainly responsible for the body metabolism and among other things and it is the place where many endogenous and exogenous substances undergo biological transformation. Lycopene is a nonprovitamin A carotenoid found in red fruits and vegetables, and its role as a potent antioxidant is well known. In this study, we hypothesized that lycopene could protect mouse liver against long-term CS exposure. Thirty C57BL/6 mice were exposed to twelve cigarette smoke (12 cigarettes per day) for 60 days and pretreated with 25 mg/kg/day or 50 mg/kg/day of lycopene via orogastric gavage. After euthanasia, the hepatic tissue was collected for histopathological, antioxidant defense, oxidative stress, inflammatory, and collagen deposition analysis. Our analysis demonstrated that lycopene results in a suitable outcome to ameliorate the pathological changes, inflammatory and antioxidant profile in a mouse model of long-term CS exposure, and collagen accumulation in the hepatic extracellular matrix. This study demonstrates for the first time that supplementation of lycopene can be a possible pharmacological tool for the treatment of hepatic damage caused by exposure to long-term CS.
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spelling pubmed-86392332021-12-03 Lycopene Ameliorates Liver Inflammation and Redox Status in Mice Exposed to Long-Term Cigarette Smoke Rocha, Daniela Fonseca Abdo Machado-Junior, Pedro Alves Souza, Ana Beatriz Farias Castro, Thalles de Freitas Costa, Guilherme de Paula Talvani, André Bezerra, Frank Silva Cangussú, Silvia Dantas Biomed Res Int Research Article Cigarette smoke (CS) is the major cause of preventable death worldwide, and it can also cause damage to extrapulmonary organs, such as the liver, mainly due the generation of reactive oxygen species (ROS). The liver is an essential organ for human survival since it is mainly responsible for the body metabolism and among other things and it is the place where many endogenous and exogenous substances undergo biological transformation. Lycopene is a nonprovitamin A carotenoid found in red fruits and vegetables, and its role as a potent antioxidant is well known. In this study, we hypothesized that lycopene could protect mouse liver against long-term CS exposure. Thirty C57BL/6 mice were exposed to twelve cigarette smoke (12 cigarettes per day) for 60 days and pretreated with 25 mg/kg/day or 50 mg/kg/day of lycopene via orogastric gavage. After euthanasia, the hepatic tissue was collected for histopathological, antioxidant defense, oxidative stress, inflammatory, and collagen deposition analysis. Our analysis demonstrated that lycopene results in a suitable outcome to ameliorate the pathological changes, inflammatory and antioxidant profile in a mouse model of long-term CS exposure, and collagen accumulation in the hepatic extracellular matrix. This study demonstrates for the first time that supplementation of lycopene can be a possible pharmacological tool for the treatment of hepatic damage caused by exposure to long-term CS. Hindawi 2021-11-25 /pmc/articles/PMC8639233/ /pubmed/34869769 http://dx.doi.org/10.1155/2021/7101313 Text en Copyright © 2021 Daniela Fonseca Abdo Rocha et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Rocha, Daniela Fonseca Abdo
Machado-Junior, Pedro Alves
Souza, Ana Beatriz Farias
Castro, Thalles de Freitas
Costa, Guilherme de Paula
Talvani, André
Bezerra, Frank Silva
Cangussú, Silvia Dantas
Lycopene Ameliorates Liver Inflammation and Redox Status in Mice Exposed to Long-Term Cigarette Smoke
title Lycopene Ameliorates Liver Inflammation and Redox Status in Mice Exposed to Long-Term Cigarette Smoke
title_full Lycopene Ameliorates Liver Inflammation and Redox Status in Mice Exposed to Long-Term Cigarette Smoke
title_fullStr Lycopene Ameliorates Liver Inflammation and Redox Status in Mice Exposed to Long-Term Cigarette Smoke
title_full_unstemmed Lycopene Ameliorates Liver Inflammation and Redox Status in Mice Exposed to Long-Term Cigarette Smoke
title_short Lycopene Ameliorates Liver Inflammation and Redox Status in Mice Exposed to Long-Term Cigarette Smoke
title_sort lycopene ameliorates liver inflammation and redox status in mice exposed to long-term cigarette smoke
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8639233/
https://www.ncbi.nlm.nih.gov/pubmed/34869769
http://dx.doi.org/10.1155/2021/7101313
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