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Thymoquinone attenuates hepatotoxicity and oxidative damage caused by diazinon: an in vivo study

Thymoquinone (TQ) is the main active constituent of Nigella sativa seeds. The objective of this study was to explore the protective effects of TQ on diazinon (DZN)-induced liver toxicity in the mouse model. The animals were divided into five groups of 6 each and treated intraperitoneally. Group 1 re...

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Autores principales: Nili-Ahmadabadi, Amir, Alibolandi, Parisa, Ranjbar, Akram, Mousavi, Leila, Nili-Ahmadabadi, Hossein, Larki-Harchegani, Amir, Ahmadimoghaddam, Davoud, Omidifar, Navid
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6288994/
https://www.ncbi.nlm.nih.gov/pubmed/30607148
http://dx.doi.org/10.4103/1735-5362.245962
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author Nili-Ahmadabadi, Amir
Alibolandi, Parisa
Ranjbar, Akram
Mousavi, Leila
Nili-Ahmadabadi, Hossein
Larki-Harchegani, Amir
Ahmadimoghaddam, Davoud
Omidifar, Navid
author_facet Nili-Ahmadabadi, Amir
Alibolandi, Parisa
Ranjbar, Akram
Mousavi, Leila
Nili-Ahmadabadi, Hossein
Larki-Harchegani, Amir
Ahmadimoghaddam, Davoud
Omidifar, Navid
author_sort Nili-Ahmadabadi, Amir
collection PubMed
description Thymoquinone (TQ) is the main active constituent of Nigella sativa seeds. The objective of this study was to explore the protective effects of TQ on diazinon (DZN)-induced liver toxicity in the mouse model. The animals were divided into five groups of 6 each and treated intraperitoneally. Group 1 received the vehicle, group 2 was given 16 mg/kg DZN, group 3 received 5 mg/kg TQ, and groups 4 and 5 were treated with 1.25 and 5 mg/kg of TQ as well as 16 mg/kg DZN, respectively. Finally, butyrylcholinesterase (BChE), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) serum activity as well as nitric oxide (NO), lipid peroxidation (LPO), total antioxidant capacity (TAC), total thiol molecule (TTM), and histopathological experiments were evaluated in the liver samples. Our findings showed that DZN caused a significant increase in ALT (P < 0.01), AST (P < 0.001), ALP (P < 0.001) serum levels, LPO (P < 0.001) and NO (P < 0.001), the depletion of the TAC (P < 0.05) and TTM (P < 0.001), and structural changes in the liver tissue. Following TQ administration, a significant improvement was observed in the oxidative stress biomarkers in the liver tissue. In addition, our biochemical findings were correlated well to the histopathological examinations. In conclusion, the data from this study indicate that the administration of TQ may prevent liver damage by preventing free radical formation in animals exposed to DZN.
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spelling pubmed-62889942019-01-03 Thymoquinone attenuates hepatotoxicity and oxidative damage caused by diazinon: an in vivo study Nili-Ahmadabadi, Amir Alibolandi, Parisa Ranjbar, Akram Mousavi, Leila Nili-Ahmadabadi, Hossein Larki-Harchegani, Amir Ahmadimoghaddam, Davoud Omidifar, Navid Res Pharm Sci Original Article Thymoquinone (TQ) is the main active constituent of Nigella sativa seeds. The objective of this study was to explore the protective effects of TQ on diazinon (DZN)-induced liver toxicity in the mouse model. The animals were divided into five groups of 6 each and treated intraperitoneally. Group 1 received the vehicle, group 2 was given 16 mg/kg DZN, group 3 received 5 mg/kg TQ, and groups 4 and 5 were treated with 1.25 and 5 mg/kg of TQ as well as 16 mg/kg DZN, respectively. Finally, butyrylcholinesterase (BChE), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) serum activity as well as nitric oxide (NO), lipid peroxidation (LPO), total antioxidant capacity (TAC), total thiol molecule (TTM), and histopathological experiments were evaluated in the liver samples. Our findings showed that DZN caused a significant increase in ALT (P < 0.01), AST (P < 0.001), ALP (P < 0.001) serum levels, LPO (P < 0.001) and NO (P < 0.001), the depletion of the TAC (P < 0.05) and TTM (P < 0.001), and structural changes in the liver tissue. Following TQ administration, a significant improvement was observed in the oxidative stress biomarkers in the liver tissue. In addition, our biochemical findings were correlated well to the histopathological examinations. In conclusion, the data from this study indicate that the administration of TQ may prevent liver damage by preventing free radical formation in animals exposed to DZN. Medknow Publications & Media Pvt Ltd 2018-12 /pmc/articles/PMC6288994/ /pubmed/30607148 http://dx.doi.org/10.4103/1735-5362.245962 Text en Copyright: © 2018 Research in Pharmaceutical Sciences http://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
Nili-Ahmadabadi, Amir
Alibolandi, Parisa
Ranjbar, Akram
Mousavi, Leila
Nili-Ahmadabadi, Hossein
Larki-Harchegani, Amir
Ahmadimoghaddam, Davoud
Omidifar, Navid
Thymoquinone attenuates hepatotoxicity and oxidative damage caused by diazinon: an in vivo study
title Thymoquinone attenuates hepatotoxicity and oxidative damage caused by diazinon: an in vivo study
title_full Thymoquinone attenuates hepatotoxicity and oxidative damage caused by diazinon: an in vivo study
title_fullStr Thymoquinone attenuates hepatotoxicity and oxidative damage caused by diazinon: an in vivo study
title_full_unstemmed Thymoquinone attenuates hepatotoxicity and oxidative damage caused by diazinon: an in vivo study
title_short Thymoquinone attenuates hepatotoxicity and oxidative damage caused by diazinon: an in vivo study
title_sort thymoquinone attenuates hepatotoxicity and oxidative damage caused by diazinon: an in vivo study
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6288994/
https://www.ncbi.nlm.nih.gov/pubmed/30607148
http://dx.doi.org/10.4103/1735-5362.245962
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