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Protective effect of rutin on the antioxidant genes expression in hypercholestrolemic male Westar rat

BACKGROUND: High-cholesterol diet (HCD) increases the oxidative stress in different tissues leading to many diseases. Rutin (RT) is a natural flavonoid (vitamin p), which possesses an antioxidant activity with protective potential. The present study aimed to examine the potential effects of rutin on...

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Autores principales: Al-Rejaie, Salem S, Aleisa, Abdulaziz M, Sayed-Ahmed, Mohamed M, AL-Shabanah, Othman A, Abuohashish, Hatem M, Ahmed, Mohammed M, Al-Hosaini, Khaled A, Hafez, Mohamed M
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3717094/
https://www.ncbi.nlm.nih.gov/pubmed/23773725
http://dx.doi.org/10.1186/1472-6882-13-136
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author Al-Rejaie, Salem S
Aleisa, Abdulaziz M
Sayed-Ahmed, Mohamed M
AL-Shabanah, Othman A
Abuohashish, Hatem M
Ahmed, Mohammed M
Al-Hosaini, Khaled A
Hafez, Mohamed M
author_facet Al-Rejaie, Salem S
Aleisa, Abdulaziz M
Sayed-Ahmed, Mohamed M
AL-Shabanah, Othman A
Abuohashish, Hatem M
Ahmed, Mohammed M
Al-Hosaini, Khaled A
Hafez, Mohamed M
author_sort Al-Rejaie, Salem S
collection PubMed
description BACKGROUND: High-cholesterol diet (HCD) increases the oxidative stress in different tissues leading to many diseases. Rutin (RT) is a natural flavonoid (vitamin p), which possesses an antioxidant activity with protective potential. The present study aimed to examine the potential effects of rutin on hypercholesterolemia-induced hepatotoxicity in rat. METHODS: Male Wistar rats were divided into four groups: GI) control (Rat chow), GII) Rutin (0.2% in rat chow), GIII) HCD (1% cholesterol and 0.5% cholic acid in rat chow) and GIV) rutin (0.2%) + HCD. RESULTS: Rutin in combination with HCD induced a significant protective effect against the hepatotoxicity by reducing the plasma level of alanine transaminase (ALT), aspartate aminotransferase (AST), triglyceride (TG), total cholesterol (TC), and low-density lipoprotein (LDL). The HCD (GII) showed a decrease in glutathione peroxidase (GPx), glutathione reductase (GR) and increase in glutathione S transferase α (GSTα), sulfiredoxin-1(Srx1), glutamate-cysteine ligase (GCL) and paraoxonase-1(PON-1) genes expression levels. CONCLUSION: Treatment with rutin reversed all the altered genes induced by HCD nearly to the control levels. The present study concluded that the HCD feedings altered the expression levels of some genes involved in the oxidative stress pathway resulting in DNA damage and hepatotoxicity. Rutin have a hepatoprotective effect through the mechanism of enhancing the antioxidant effect via amelioration of oxidative stress genes.
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spelling pubmed-37170942013-07-21 Protective effect of rutin on the antioxidant genes expression in hypercholestrolemic male Westar rat Al-Rejaie, Salem S Aleisa, Abdulaziz M Sayed-Ahmed, Mohamed M AL-Shabanah, Othman A Abuohashish, Hatem M Ahmed, Mohammed M Al-Hosaini, Khaled A Hafez, Mohamed M BMC Complement Altern Med Research Article BACKGROUND: High-cholesterol diet (HCD) increases the oxidative stress in different tissues leading to many diseases. Rutin (RT) is a natural flavonoid (vitamin p), which possesses an antioxidant activity with protective potential. The present study aimed to examine the potential effects of rutin on hypercholesterolemia-induced hepatotoxicity in rat. METHODS: Male Wistar rats were divided into four groups: GI) control (Rat chow), GII) Rutin (0.2% in rat chow), GIII) HCD (1% cholesterol and 0.5% cholic acid in rat chow) and GIV) rutin (0.2%) + HCD. RESULTS: Rutin in combination with HCD induced a significant protective effect against the hepatotoxicity by reducing the plasma level of alanine transaminase (ALT), aspartate aminotransferase (AST), triglyceride (TG), total cholesterol (TC), and low-density lipoprotein (LDL). The HCD (GII) showed a decrease in glutathione peroxidase (GPx), glutathione reductase (GR) and increase in glutathione S transferase α (GSTα), sulfiredoxin-1(Srx1), glutamate-cysteine ligase (GCL) and paraoxonase-1(PON-1) genes expression levels. CONCLUSION: Treatment with rutin reversed all the altered genes induced by HCD nearly to the control levels. The present study concluded that the HCD feedings altered the expression levels of some genes involved in the oxidative stress pathway resulting in DNA damage and hepatotoxicity. Rutin have a hepatoprotective effect through the mechanism of enhancing the antioxidant effect via amelioration of oxidative stress genes. BioMed Central 2013-06-17 /pmc/articles/PMC3717094/ /pubmed/23773725 http://dx.doi.org/10.1186/1472-6882-13-136 Text en Copyright © 2013 Al-Rejaie et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Al-Rejaie, Salem S
Aleisa, Abdulaziz M
Sayed-Ahmed, Mohamed M
AL-Shabanah, Othman A
Abuohashish, Hatem M
Ahmed, Mohammed M
Al-Hosaini, Khaled A
Hafez, Mohamed M
Protective effect of rutin on the antioxidant genes expression in hypercholestrolemic male Westar rat
title Protective effect of rutin on the antioxidant genes expression in hypercholestrolemic male Westar rat
title_full Protective effect of rutin on the antioxidant genes expression in hypercholestrolemic male Westar rat
title_fullStr Protective effect of rutin on the antioxidant genes expression in hypercholestrolemic male Westar rat
title_full_unstemmed Protective effect of rutin on the antioxidant genes expression in hypercholestrolemic male Westar rat
title_short Protective effect of rutin on the antioxidant genes expression in hypercholestrolemic male Westar rat
title_sort protective effect of rutin on the antioxidant genes expression in hypercholestrolemic male westar rat
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3717094/
https://www.ncbi.nlm.nih.gov/pubmed/23773725
http://dx.doi.org/10.1186/1472-6882-13-136
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