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Effects of phloretin on oxidative and inflammatory reaction in rat model of cecal ligation and puncture induced sepsis

BACKGROUND: Sepsis is a debilitating systemic disease and described as a severe and irregular systemic inflammatory reaction syndrome (SIRS) against infection. We employed CLP (Cecal Ligation and Puncture) model in rats to investigate anti-inflammatory and antioxidant effects of phloretin, as a natu...

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Autores principales: Aliomrani, Mehdi, Sepand, Mohammad Reza, Mirzaei, Hamid Reza, kazemi, Ali Reza, Nekonam, Saeid, Sabzevari, Omid
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4858854/
https://www.ncbi.nlm.nih.gov/pubmed/27150961
http://dx.doi.org/10.1186/s40199-016-0154-9
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author Aliomrani, Mehdi
Sepand, Mohammad Reza
Mirzaei, Hamid Reza
kazemi, Ali Reza
Nekonam, Saeid
Sabzevari, Omid
author_facet Aliomrani, Mehdi
Sepand, Mohammad Reza
Mirzaei, Hamid Reza
kazemi, Ali Reza
Nekonam, Saeid
Sabzevari, Omid
author_sort Aliomrani, Mehdi
collection PubMed
description BACKGROUND: Sepsis is a debilitating systemic disease and described as a severe and irregular systemic inflammatory reaction syndrome (SIRS) against infection. We employed CLP (Cecal Ligation and Puncture) model in rats to investigate anti-inflammatory and antioxidant effects of phloretin, as a natural antioxidant agent, and its protective effect on liver tissue damage caused by sepsis. METHODS: Male Wistar albino rats were randomly divided into three groups: sham group, CLP induced sepsis group and phloretin treated CLP group. Sepsis was induced by CLP method. 50 mmol/kg Phloretin was administered intraperitoneally in two equal doses immediately after surgery. RESULTS: It was observed that blood urea nitrogen (BUN) and tumor necrosis factor alpha (TNF-α) levels were dramatically increased in the CLP induced sepsis group (43.88 ± 1.905 mg/dl, 37.63 ± 1.92, respectively) when compared to the sham group. Moreover, tissue Glutathione (GSH) and liver nuclear factor ĸB (NF-ĸB p65) transcription factor values were higher in CLP induced sepsis group. This elevation was considerably reduced in the phloretin treated CLP group. No significant differences were observed in serum creatinine and creatinine phosphokinase levels. CONCLUSIONS: The present study suggested that phloretin, as a natural protective agent, act against tissue damages introduced following the experimental sepsis induced model, likely caused by free oxygen radicals.
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spelling pubmed-48588542016-05-07 Effects of phloretin on oxidative and inflammatory reaction in rat model of cecal ligation and puncture induced sepsis Aliomrani, Mehdi Sepand, Mohammad Reza Mirzaei, Hamid Reza kazemi, Ali Reza Nekonam, Saeid Sabzevari, Omid Daru Research Article BACKGROUND: Sepsis is a debilitating systemic disease and described as a severe and irregular systemic inflammatory reaction syndrome (SIRS) against infection. We employed CLP (Cecal Ligation and Puncture) model in rats to investigate anti-inflammatory and antioxidant effects of phloretin, as a natural antioxidant agent, and its protective effect on liver tissue damage caused by sepsis. METHODS: Male Wistar albino rats were randomly divided into three groups: sham group, CLP induced sepsis group and phloretin treated CLP group. Sepsis was induced by CLP method. 50 mmol/kg Phloretin was administered intraperitoneally in two equal doses immediately after surgery. RESULTS: It was observed that blood urea nitrogen (BUN) and tumor necrosis factor alpha (TNF-α) levels were dramatically increased in the CLP induced sepsis group (43.88 ± 1.905 mg/dl, 37.63 ± 1.92, respectively) when compared to the sham group. Moreover, tissue Glutathione (GSH) and liver nuclear factor ĸB (NF-ĸB p65) transcription factor values were higher in CLP induced sepsis group. This elevation was considerably reduced in the phloretin treated CLP group. No significant differences were observed in serum creatinine and creatinine phosphokinase levels. CONCLUSIONS: The present study suggested that phloretin, as a natural protective agent, act against tissue damages introduced following the experimental sepsis induced model, likely caused by free oxygen radicals. BioMed Central 2016-05-06 /pmc/articles/PMC4858854/ /pubmed/27150961 http://dx.doi.org/10.1186/s40199-016-0154-9 Text en © Aliomrani et al. 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Aliomrani, Mehdi
Sepand, Mohammad Reza
Mirzaei, Hamid Reza
kazemi, Ali Reza
Nekonam, Saeid
Sabzevari, Omid
Effects of phloretin on oxidative and inflammatory reaction in rat model of cecal ligation and puncture induced sepsis
title Effects of phloretin on oxidative and inflammatory reaction in rat model of cecal ligation and puncture induced sepsis
title_full Effects of phloretin on oxidative and inflammatory reaction in rat model of cecal ligation and puncture induced sepsis
title_fullStr Effects of phloretin on oxidative and inflammatory reaction in rat model of cecal ligation and puncture induced sepsis
title_full_unstemmed Effects of phloretin on oxidative and inflammatory reaction in rat model of cecal ligation and puncture induced sepsis
title_short Effects of phloretin on oxidative and inflammatory reaction in rat model of cecal ligation and puncture induced sepsis
title_sort effects of phloretin on oxidative and inflammatory reaction in rat model of cecal ligation and puncture induced sepsis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4858854/
https://www.ncbi.nlm.nih.gov/pubmed/27150961
http://dx.doi.org/10.1186/s40199-016-0154-9
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