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Role of Ferulic Acid in the Amelioration of Ionizing Radiation Induced Inflammation: A Murine Model

Ionizing radiation is responsible for oxidative stress by generating reactive oxygen species (ROS), which alters the cellular redox potential. This change activates several redox sensitive enzymes which are crucial in activating signaling pathways at molecular level and can lead to oxidative stress...

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Autores principales: Das, Ujjal, Manna, Krishnendu, Sinha, Mahuya, Datta, Sanjukta, Das, Dipesh Kr, Chakraborty, Anindita, Ghosh, Mahua, Saha, Krishna Das, Dey, Sanjit
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031149/
https://www.ncbi.nlm.nih.gov/pubmed/24854039
http://dx.doi.org/10.1371/journal.pone.0097599
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author Das, Ujjal
Manna, Krishnendu
Sinha, Mahuya
Datta, Sanjukta
Das, Dipesh Kr
Chakraborty, Anindita
Ghosh, Mahua
Saha, Krishna Das
Dey, Sanjit
author_facet Das, Ujjal
Manna, Krishnendu
Sinha, Mahuya
Datta, Sanjukta
Das, Dipesh Kr
Chakraborty, Anindita
Ghosh, Mahua
Saha, Krishna Das
Dey, Sanjit
author_sort Das, Ujjal
collection PubMed
description Ionizing radiation is responsible for oxidative stress by generating reactive oxygen species (ROS), which alters the cellular redox potential. This change activates several redox sensitive enzymes which are crucial in activating signaling pathways at molecular level and can lead to oxidative stress induced inflammation. Therefore, the present study was intended to assess the anti-inflammatory role of ferulic acid (FA), a plant flavonoid, against radiation-induced oxidative stress with a novel mechanistic viewpoint. FA was administered (50 mg/kg body wt) to Swiss albino mice for five consecutive days prior to exposing them to a single dose of 10 Gy (60)Co γ-irradiation. The dose of FA was optimized from the survival experiment and 50 mg/kg body wt dose showed optimum effect. FA significantly ameliorated the radiation induced inflammatory response such as phosphorylation of IKKα/β and IκBα and consequent nuclear translocation of nuclear factor kappa B (NF-κB). FA also prevented the increase of cycloxygenase-2 (Cox-2) protein, inducible nitric oxide synthase-2 (iNOS-2) gene expression, lipid peroxidation in liver and the increase of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in serum. It was observed that exposure to radiation results in decreased activity of superoxide dismutase (SOD), catalase (CAT) and the pool of reduced glutathione (GSH) content. However, FA treatment prior to irradiation increased the activities of the same endogenous antioxidants. Thus, pretreatment with FA offers protection against gamma radiation induced inflammation.
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spelling pubmed-40311492014-05-28 Role of Ferulic Acid in the Amelioration of Ionizing Radiation Induced Inflammation: A Murine Model Das, Ujjal Manna, Krishnendu Sinha, Mahuya Datta, Sanjukta Das, Dipesh Kr Chakraborty, Anindita Ghosh, Mahua Saha, Krishna Das Dey, Sanjit PLoS One Research Article Ionizing radiation is responsible for oxidative stress by generating reactive oxygen species (ROS), which alters the cellular redox potential. This change activates several redox sensitive enzymes which are crucial in activating signaling pathways at molecular level and can lead to oxidative stress induced inflammation. Therefore, the present study was intended to assess the anti-inflammatory role of ferulic acid (FA), a plant flavonoid, against radiation-induced oxidative stress with a novel mechanistic viewpoint. FA was administered (50 mg/kg body wt) to Swiss albino mice for five consecutive days prior to exposing them to a single dose of 10 Gy (60)Co γ-irradiation. The dose of FA was optimized from the survival experiment and 50 mg/kg body wt dose showed optimum effect. FA significantly ameliorated the radiation induced inflammatory response such as phosphorylation of IKKα/β and IκBα and consequent nuclear translocation of nuclear factor kappa B (NF-κB). FA also prevented the increase of cycloxygenase-2 (Cox-2) protein, inducible nitric oxide synthase-2 (iNOS-2) gene expression, lipid peroxidation in liver and the increase of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in serum. It was observed that exposure to radiation results in decreased activity of superoxide dismutase (SOD), catalase (CAT) and the pool of reduced glutathione (GSH) content. However, FA treatment prior to irradiation increased the activities of the same endogenous antioxidants. Thus, pretreatment with FA offers protection against gamma radiation induced inflammation. Public Library of Science 2014-05-22 /pmc/articles/PMC4031149/ /pubmed/24854039 http://dx.doi.org/10.1371/journal.pone.0097599 Text en © 2014 Das et al 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 author and source are properly credited.
spellingShingle Research Article
Das, Ujjal
Manna, Krishnendu
Sinha, Mahuya
Datta, Sanjukta
Das, Dipesh Kr
Chakraborty, Anindita
Ghosh, Mahua
Saha, Krishna Das
Dey, Sanjit
Role of Ferulic Acid in the Amelioration of Ionizing Radiation Induced Inflammation: A Murine Model
title Role of Ferulic Acid in the Amelioration of Ionizing Radiation Induced Inflammation: A Murine Model
title_full Role of Ferulic Acid in the Amelioration of Ionizing Radiation Induced Inflammation: A Murine Model
title_fullStr Role of Ferulic Acid in the Amelioration of Ionizing Radiation Induced Inflammation: A Murine Model
title_full_unstemmed Role of Ferulic Acid in the Amelioration of Ionizing Radiation Induced Inflammation: A Murine Model
title_short Role of Ferulic Acid in the Amelioration of Ionizing Radiation Induced Inflammation: A Murine Model
title_sort role of ferulic acid in the amelioration of ionizing radiation induced inflammation: a murine model
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031149/
https://www.ncbi.nlm.nih.gov/pubmed/24854039
http://dx.doi.org/10.1371/journal.pone.0097599
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