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Protective Effects of Flavone from Tamarix aphylla against CCl(4)-Induced Liver Injury in Mice Mediated by Suppression of Oxidative Stress, Apoptosis and Angiogenesis
The current study aimed to investigate, for the first time, the beneficial effects of 3,5-dihydroxy-4′,7-dimethoxyflavone isolated from Tamarix aphylla L. against liver injury in mice. Liver injury was induced by intraperitoneal (i.p.) injection of carbon tetrachloride (CCl(4)) at a dose of 0.4 mL/k...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6829218/ https://www.ncbi.nlm.nih.gov/pubmed/31640181 http://dx.doi.org/10.3390/ijms20205215 |
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author | El-Aarag, Bishoy Khairy, Asmaa Khalifa, Shaden A. M. El-Seedi, Hesham R. |
author_facet | El-Aarag, Bishoy Khairy, Asmaa Khalifa, Shaden A. M. El-Seedi, Hesham R. |
author_sort | El-Aarag, Bishoy |
collection | PubMed |
description | The current study aimed to investigate, for the first time, the beneficial effects of 3,5-dihydroxy-4′,7-dimethoxyflavone isolated from Tamarix aphylla L. against liver injury in mice. Liver injury was induced by intraperitoneal (i.p.) injection of carbon tetrachloride (CCl(4)) at a dose of 0.4 mL/kg mixed in olive oil at ratio (1:4) twice a week for 6 consecutive weeks. The administration of CCl(4) caused significant histopathological changes in liver tissues while the pre-treatment with the flavone at dose of 10 and 25 mg/kg ameliorated the observed liver damages. Also, it markedly reduced hepatic malondialdehyde (MDA) level as well as increased the activities of liver superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (Gpx) compared with their recorded levels in CCl(4) model group. Moreover, the immunohistochemical analysis demonstrated the enhancement in the protein level of B-cell lymphoma-2 (Bcl-2) while the protein levels of cysteine-aspartic acid protease-3 (caspase-3), Bcl-2-associated x protein (Bax), transforming growth factor-β1 (TGF-β1) and CD31 were suppressed following the flavone treatement. These results suggest that the flavone can inhibit liver injury induced in mice owning to its impact on the oxidation, apoptotic and angiogenesis mechanisms. Further pharmacological investigations are essential to determine the effectiveness of the flavone in human. |
format | Online Article Text |
id | pubmed-6829218 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-68292182019-11-18 Protective Effects of Flavone from Tamarix aphylla against CCl(4)-Induced Liver Injury in Mice Mediated by Suppression of Oxidative Stress, Apoptosis and Angiogenesis El-Aarag, Bishoy Khairy, Asmaa Khalifa, Shaden A. M. El-Seedi, Hesham R. Int J Mol Sci Article The current study aimed to investigate, for the first time, the beneficial effects of 3,5-dihydroxy-4′,7-dimethoxyflavone isolated from Tamarix aphylla L. against liver injury in mice. Liver injury was induced by intraperitoneal (i.p.) injection of carbon tetrachloride (CCl(4)) at a dose of 0.4 mL/kg mixed in olive oil at ratio (1:4) twice a week for 6 consecutive weeks. The administration of CCl(4) caused significant histopathological changes in liver tissues while the pre-treatment with the flavone at dose of 10 and 25 mg/kg ameliorated the observed liver damages. Also, it markedly reduced hepatic malondialdehyde (MDA) level as well as increased the activities of liver superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (Gpx) compared with their recorded levels in CCl(4) model group. Moreover, the immunohistochemical analysis demonstrated the enhancement in the protein level of B-cell lymphoma-2 (Bcl-2) while the protein levels of cysteine-aspartic acid protease-3 (caspase-3), Bcl-2-associated x protein (Bax), transforming growth factor-β1 (TGF-β1) and CD31 were suppressed following the flavone treatement. These results suggest that the flavone can inhibit liver injury induced in mice owning to its impact on the oxidation, apoptotic and angiogenesis mechanisms. Further pharmacological investigations are essential to determine the effectiveness of the flavone in human. MDPI 2019-10-21 /pmc/articles/PMC6829218/ /pubmed/31640181 http://dx.doi.org/10.3390/ijms20205215 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article El-Aarag, Bishoy Khairy, Asmaa Khalifa, Shaden A. M. El-Seedi, Hesham R. Protective Effects of Flavone from Tamarix aphylla against CCl(4)-Induced Liver Injury in Mice Mediated by Suppression of Oxidative Stress, Apoptosis and Angiogenesis |
title | Protective Effects of Flavone from Tamarix aphylla against CCl(4)-Induced Liver Injury in Mice Mediated by Suppression of Oxidative Stress, Apoptosis and Angiogenesis |
title_full | Protective Effects of Flavone from Tamarix aphylla against CCl(4)-Induced Liver Injury in Mice Mediated by Suppression of Oxidative Stress, Apoptosis and Angiogenesis |
title_fullStr | Protective Effects of Flavone from Tamarix aphylla against CCl(4)-Induced Liver Injury in Mice Mediated by Suppression of Oxidative Stress, Apoptosis and Angiogenesis |
title_full_unstemmed | Protective Effects of Flavone from Tamarix aphylla against CCl(4)-Induced Liver Injury in Mice Mediated by Suppression of Oxidative Stress, Apoptosis and Angiogenesis |
title_short | Protective Effects of Flavone from Tamarix aphylla against CCl(4)-Induced Liver Injury in Mice Mediated by Suppression of Oxidative Stress, Apoptosis and Angiogenesis |
title_sort | protective effects of flavone from tamarix aphylla against ccl(4)-induced liver injury in mice mediated by suppression of oxidative stress, apoptosis and angiogenesis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6829218/ https://www.ncbi.nlm.nih.gov/pubmed/31640181 http://dx.doi.org/10.3390/ijms20205215 |
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