Eugenol Administration Improves Liver Damage Induced by a Fructose-Rich Diet

BACKGROUNDS: The prevalence of metabolic syndrome (MetS) is increasing in developing countries that affects the liver in a variety of ways. This study was designed to investigate the protective role of eugenol on liver damage caused by fructose-induced MetS. MATERIALS AND METHODS: Thirty male Wistar...

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Autores principales: Niazi, Abbass Ali, Kourkinejad Gharaei, Fatemeh, Saebinasab, Zahra, Maleki, Maryam, Maghool, Fatemeh, Fereidooni, Fatemeh, Safari, Tahereh
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer - Medknow 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8744418/
https://www.ncbi.nlm.nih.gov/pubmed/35071110
http://dx.doi.org/10.4103/abr.abr_237_20
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author Niazi, Abbass Ali
Kourkinejad Gharaei, Fatemeh
Saebinasab, Zahra
Maleki, Maryam
Maghool, Fatemeh
Fereidooni, Fatemeh
Safari, Tahereh
author_facet Niazi, Abbass Ali
Kourkinejad Gharaei, Fatemeh
Saebinasab, Zahra
Maleki, Maryam
Maghool, Fatemeh
Fereidooni, Fatemeh
Safari, Tahereh
author_sort Niazi, Abbass Ali
collection PubMed
description BACKGROUNDS: The prevalence of metabolic syndrome (MetS) is increasing in developing countries that affects the liver in a variety of ways. This study was designed to investigate the protective role of eugenol on liver damage caused by fructose-induced MetS. MATERIALS AND METHODS: Thirty male Wistar rats were randomly divided into five groups: 1: tap water (control), 2: fructose, 3: fructose + eugenol solvent, 4: fructose + eugenol 50 mg/kg, and 5: fructose + eugenol 100 mg/kg. At the end of the experiment, blood samples were taken for measurement fast blood glucose (FBG), serum glutamic-oxaloacetic transaminase (SGOT), serum glutamic pyruvate transaminase (SGPT), low-density lipoprotein, high-density lipoprotein, cholesterol, and triglyceride. RESULTS: FBG significantly increased in Group 2 compared to Group 1 (P < 0.001); however, it significantly decreased in Groups 4 and 5 compared to Group 2 (P < 0.05). SGOT and SGPT levels significantly increased in Group 2 compared to the control group (P < 0.001). However, SGOT and SGPT levels significantly decreased in Groups 4 and 5. Malondialdehyde (MDA) and liver tissue damage score (LTDS) significantly increased in Group 2 compared with the control group (P < 0.01), whereas MDA and LTDS decreased in Groups 4 and 5 compared to Group 2 (P < 0.05). CONCLUSION: Eugenol may ameliorate liver damage in a rat model of fructose-induced MetS, and these protective effects may in part be mediated by improving antioxidant status and reducing oxidative stress and lipid peroxidation. It may also reduce hepatic inflammation and fat accumulation as well as fibrosis of liver cells.
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spelling pubmed-87444182022-01-21 Eugenol Administration Improves Liver Damage Induced by a Fructose-Rich Diet Niazi, Abbass Ali Kourkinejad Gharaei, Fatemeh Saebinasab, Zahra Maleki, Maryam Maghool, Fatemeh Fereidooni, Fatemeh Safari, Tahereh Adv Biomed Res Original Article BACKGROUNDS: The prevalence of metabolic syndrome (MetS) is increasing in developing countries that affects the liver in a variety of ways. This study was designed to investigate the protective role of eugenol on liver damage caused by fructose-induced MetS. MATERIALS AND METHODS: Thirty male Wistar rats were randomly divided into five groups: 1: tap water (control), 2: fructose, 3: fructose + eugenol solvent, 4: fructose + eugenol 50 mg/kg, and 5: fructose + eugenol 100 mg/kg. At the end of the experiment, blood samples were taken for measurement fast blood glucose (FBG), serum glutamic-oxaloacetic transaminase (SGOT), serum glutamic pyruvate transaminase (SGPT), low-density lipoprotein, high-density lipoprotein, cholesterol, and triglyceride. RESULTS: FBG significantly increased in Group 2 compared to Group 1 (P < 0.001); however, it significantly decreased in Groups 4 and 5 compared to Group 2 (P < 0.05). SGOT and SGPT levels significantly increased in Group 2 compared to the control group (P < 0.001). However, SGOT and SGPT levels significantly decreased in Groups 4 and 5. Malondialdehyde (MDA) and liver tissue damage score (LTDS) significantly increased in Group 2 compared with the control group (P < 0.01), whereas MDA and LTDS decreased in Groups 4 and 5 compared to Group 2 (P < 0.05). CONCLUSION: Eugenol may ameliorate liver damage in a rat model of fructose-induced MetS, and these protective effects may in part be mediated by improving antioxidant status and reducing oxidative stress and lipid peroxidation. It may also reduce hepatic inflammation and fat accumulation as well as fibrosis of liver cells. Wolters Kluwer - Medknow 2021-11-26 /pmc/articles/PMC8744418/ /pubmed/35071110 http://dx.doi.org/10.4103/abr.abr_237_20 Text en Copyright: © 2021 Advanced Biomedical Research https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.
spellingShingle Original Article
Niazi, Abbass Ali
Kourkinejad Gharaei, Fatemeh
Saebinasab, Zahra
Maleki, Maryam
Maghool, Fatemeh
Fereidooni, Fatemeh
Safari, Tahereh
Eugenol Administration Improves Liver Damage Induced by a Fructose-Rich Diet
title Eugenol Administration Improves Liver Damage Induced by a Fructose-Rich Diet
title_full Eugenol Administration Improves Liver Damage Induced by a Fructose-Rich Diet
title_fullStr Eugenol Administration Improves Liver Damage Induced by a Fructose-Rich Diet
title_full_unstemmed Eugenol Administration Improves Liver Damage Induced by a Fructose-Rich Diet
title_short Eugenol Administration Improves Liver Damage Induced by a Fructose-Rich Diet
title_sort eugenol administration improves liver damage induced by a fructose-rich diet
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8744418/
https://www.ncbi.nlm.nih.gov/pubmed/35071110
http://dx.doi.org/10.4103/abr.abr_237_20
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