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Diclofenac – induced hepatotoxicity: Low dose of omega-3 fatty acids have more protective effects
The global embrace of the Western dietary style has necessitated the need for supplementation with omega-3 fatty acids (N-3) to redress the imbalance in omega-6/omega-3 fatty acids ratio. Therefore, the study investigated the effects of pre-treatment with N-3 in adult male Wistar rats exposed to dic...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2017
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5977161/ https://www.ncbi.nlm.nih.gov/pubmed/29854580 http://dx.doi.org/10.1016/j.toxrep.2017.12.002 |
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author | Adeyemi, Wale Johnson Olayaki, Luqman Aribidesi |
author_facet | Adeyemi, Wale Johnson Olayaki, Luqman Aribidesi |
author_sort | Adeyemi, Wale Johnson |
collection | PubMed |
description | The global embrace of the Western dietary style has necessitated the need for supplementation with omega-3 fatty acids (N-3) to redress the imbalance in omega-6/omega-3 fatty acids ratio. Therefore, the study investigated the effects of pre-treatment with N-3 in adult male Wistar rats exposed to diclofenac sodium (DF). Twenty adult male Wistar rats were used for this study. They were divided into 4 groups of 5 rats each, which included: Group 1 - Normal control; Group 2 - DF control; Group 3 - Low N-3 + DF; and, Group 4 - High N-3 + DF. The rats in group 2 were administered DF (10 mg/kg b.w./day, im) during the last 7 days of the experiment, while the rats in groups 3 and 4 were pre-treated with N-3 at 100 and 300 mg/kg b.w./day, po respectively for 21 days, afterwards, they received DF at 10 mg/kg b.w./day (im) for 7 days. The result showed that DF significantly increased malondialdehyde, lactate dehydrogenase, and pro-inflammatory markers (total white blood cell count, uric acid, platelet/lymphocyte and neutrophil/lymphocyte ratios). Moreover, DF significantly elevated the activities of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase, but, significant reduced the total antioxidant capacity and the activities of superoxide dismutase, catalase, and glutathione peroxidase. The histological results were parallel to the biochemical and haematological findings. Pre-treatment with N-3 significantly prevented the manifestation of the abnormalities brought about by DF. Although there were indications of the dose-dependent effects of N-3, the low dose was found to be more effective. In conclusion, the pre-administration of N-3, preferably at a low dose, could reduce hepatotoxicity that could result from subsequent exposure to DF. |
format | Online Article Text |
id | pubmed-5977161 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-59771612018-05-31 Diclofenac – induced hepatotoxicity: Low dose of omega-3 fatty acids have more protective effects Adeyemi, Wale Johnson Olayaki, Luqman Aribidesi Toxicol Rep Article The global embrace of the Western dietary style has necessitated the need for supplementation with omega-3 fatty acids (N-3) to redress the imbalance in omega-6/omega-3 fatty acids ratio. Therefore, the study investigated the effects of pre-treatment with N-3 in adult male Wistar rats exposed to diclofenac sodium (DF). Twenty adult male Wistar rats were used for this study. They were divided into 4 groups of 5 rats each, which included: Group 1 - Normal control; Group 2 - DF control; Group 3 - Low N-3 + DF; and, Group 4 - High N-3 + DF. The rats in group 2 were administered DF (10 mg/kg b.w./day, im) during the last 7 days of the experiment, while the rats in groups 3 and 4 were pre-treated with N-3 at 100 and 300 mg/kg b.w./day, po respectively for 21 days, afterwards, they received DF at 10 mg/kg b.w./day (im) for 7 days. The result showed that DF significantly increased malondialdehyde, lactate dehydrogenase, and pro-inflammatory markers (total white blood cell count, uric acid, platelet/lymphocyte and neutrophil/lymphocyte ratios). Moreover, DF significantly elevated the activities of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase, but, significant reduced the total antioxidant capacity and the activities of superoxide dismutase, catalase, and glutathione peroxidase. The histological results were parallel to the biochemical and haematological findings. Pre-treatment with N-3 significantly prevented the manifestation of the abnormalities brought about by DF. Although there were indications of the dose-dependent effects of N-3, the low dose was found to be more effective. In conclusion, the pre-administration of N-3, preferably at a low dose, could reduce hepatotoxicity that could result from subsequent exposure to DF. Elsevier 2017-12-16 /pmc/articles/PMC5977161/ /pubmed/29854580 http://dx.doi.org/10.1016/j.toxrep.2017.12.002 Text en © 2017 Published by Elsevier Ireland Ltd. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Article Adeyemi, Wale Johnson Olayaki, Luqman Aribidesi Diclofenac – induced hepatotoxicity: Low dose of omega-3 fatty acids have more protective effects |
title | Diclofenac – induced hepatotoxicity: Low dose of omega-3 fatty acids have more protective effects |
title_full | Diclofenac – induced hepatotoxicity: Low dose of omega-3 fatty acids have more protective effects |
title_fullStr | Diclofenac – induced hepatotoxicity: Low dose of omega-3 fatty acids have more protective effects |
title_full_unstemmed | Diclofenac – induced hepatotoxicity: Low dose of omega-3 fatty acids have more protective effects |
title_short | Diclofenac – induced hepatotoxicity: Low dose of omega-3 fatty acids have more protective effects |
title_sort | diclofenac – induced hepatotoxicity: low dose of omega-3 fatty acids have more protective effects |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5977161/ https://www.ncbi.nlm.nih.gov/pubmed/29854580 http://dx.doi.org/10.1016/j.toxrep.2017.12.002 |
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