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Protective effect of pretreatment with thymoquinone against Aflatoxin B(1) induced liver toxicity in mice

BACKGROUND AND THE PURPOSE OF THE STUDY: Thymoquinone (TQ) is one of the active components of Nigella sativa. The plant has been used in herbal medicine for treatment of many diseases including liver complications. The present study aimed to investigate protective effects of TQ on Aflatoxin B(1) (AF...

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Autores principales: Nili-Ahmadabadi, A., Tavakoli, F., Hasanzadeh, GR., Rahimi, HR., Sabzevari, O.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Tehran University of Medical Sciences 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3304388/
https://www.ncbi.nlm.nih.gov/pubmed/22615670
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author Nili-Ahmadabadi, A.
Tavakoli, F.
Hasanzadeh, GR.
Rahimi, HR.
Sabzevari, O.
author_facet Nili-Ahmadabadi, A.
Tavakoli, F.
Hasanzadeh, GR.
Rahimi, HR.
Sabzevari, O.
author_sort Nili-Ahmadabadi, A.
collection PubMed
description BACKGROUND AND THE PURPOSE OF THE STUDY: Thymoquinone (TQ) is one of the active components of Nigella sativa. The plant has been used in herbal medicine for treatment of many diseases including liver complications. The present study aimed to investigate protective effects of TQ on Aflatoxin B(1) (AFB(1)) induced liver toxicity in mice. METHODS: Animals were divided into six groups and treated intraperitoneally. Group 1 (blank) served as vehicle, group 2 (positive control) received AFB(1), Group 3 was treated with 9 mg/kg of TQ, Groups 4, 5 and 6 were treated with 4.5, 9 and 18 mg/kg of TQ, respectively. After three consecutive days, except for groups 1 and 3, animals were administered with a single dose of AFB(1) (2 mg/kg). All the animals were killed 24 hrs following the AFB(1) administration under ether anesthesia. Biochemical parameters including AST, ALT and ALP in serum samples and glutathione (GSH) and malondialdehyde (MDA) contents in liver homogenates were determined. Liver sections were collected for histopathological examination. RESULTS: Findings of this study showed that AST, ALT, ALP and MDA levels were significantly lower in the TQ treated animals as compared to AFB(1) group (group 2). Furthermore, TQ was able to recover glutathione content (GSH) of liver tissue. The best response, however, was observed with the dose of 9 mg/kg. Liver sections of AFB(1) intoxicated mice showed inflammation, necrosis, hyperplasia of kupffer and infiltration of mononuclear cells, dilation of sinusoids and disruption of hepatocytes, while treatment with TQ helped to normalize liver architecture in accordance to biochemical findings. CONCLUSION: Taken collectively, TQ has a protective role with optimum dose of 9 mg/kg in AFB(1) hepatotoxicity.
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spelling pubmed-33043882012-05-21 Protective effect of pretreatment with thymoquinone against Aflatoxin B(1) induced liver toxicity in mice Nili-Ahmadabadi, A. Tavakoli, F. Hasanzadeh, GR. Rahimi, HR. Sabzevari, O. Daru Original Article BACKGROUND AND THE PURPOSE OF THE STUDY: Thymoquinone (TQ) is one of the active components of Nigella sativa. The plant has been used in herbal medicine for treatment of many diseases including liver complications. The present study aimed to investigate protective effects of TQ on Aflatoxin B(1) (AFB(1)) induced liver toxicity in mice. METHODS: Animals were divided into six groups and treated intraperitoneally. Group 1 (blank) served as vehicle, group 2 (positive control) received AFB(1), Group 3 was treated with 9 mg/kg of TQ, Groups 4, 5 and 6 were treated with 4.5, 9 and 18 mg/kg of TQ, respectively. After three consecutive days, except for groups 1 and 3, animals were administered with a single dose of AFB(1) (2 mg/kg). All the animals were killed 24 hrs following the AFB(1) administration under ether anesthesia. Biochemical parameters including AST, ALT and ALP in serum samples and glutathione (GSH) and malondialdehyde (MDA) contents in liver homogenates were determined. Liver sections were collected for histopathological examination. RESULTS: Findings of this study showed that AST, ALT, ALP and MDA levels were significantly lower in the TQ treated animals as compared to AFB(1) group (group 2). Furthermore, TQ was able to recover glutathione content (GSH) of liver tissue. The best response, however, was observed with the dose of 9 mg/kg. Liver sections of AFB(1) intoxicated mice showed inflammation, necrosis, hyperplasia of kupffer and infiltration of mononuclear cells, dilation of sinusoids and disruption of hepatocytes, while treatment with TQ helped to normalize liver architecture in accordance to biochemical findings. CONCLUSION: Taken collectively, TQ has a protective role with optimum dose of 9 mg/kg in AFB(1) hepatotoxicity. Tehran University of Medical Sciences 2011 /pmc/articles/PMC3304388/ /pubmed/22615670 Text en © 2011 Tehran University of Medical Sciences http://creativecommons.org/licenses/by-nc/3.0/ This work is licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License which allows users to read, copy, distribute and make derivative works for non-commercial purposes from the material, as long as the author of the original work is cited properly.
spellingShingle Original Article
Nili-Ahmadabadi, A.
Tavakoli, F.
Hasanzadeh, GR.
Rahimi, HR.
Sabzevari, O.
Protective effect of pretreatment with thymoquinone against Aflatoxin B(1) induced liver toxicity in mice
title Protective effect of pretreatment with thymoquinone against Aflatoxin B(1) induced liver toxicity in mice
title_full Protective effect of pretreatment with thymoquinone against Aflatoxin B(1) induced liver toxicity in mice
title_fullStr Protective effect of pretreatment with thymoquinone against Aflatoxin B(1) induced liver toxicity in mice
title_full_unstemmed Protective effect of pretreatment with thymoquinone against Aflatoxin B(1) induced liver toxicity in mice
title_short Protective effect of pretreatment with thymoquinone against Aflatoxin B(1) induced liver toxicity in mice
title_sort protective effect of pretreatment with thymoquinone against aflatoxin b(1) induced liver toxicity in mice
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3304388/
https://www.ncbi.nlm.nih.gov/pubmed/22615670
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