Potential Therapeutic Role of Osteopontin Inhibition in Liver Fibrosis -Induced by Thioacetamide in Rats

To examine the effect of osteopontin inhibition by tranilast on liver fibrosis, four groups of rats were used throughout this study. Group I (Control group): rats received the solvent. Liver fibrosis was induced in Groups II, III, and IV by thioacetamide (TAA; 200mg/kg, ip) twice weekly for 6 weeks....

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Autores principales: Ramadan A., Nehal A. Afifi, Nemat Z. Yassin, Rehab F. Abdel-Rahman, Sahar S. Abd El-Rahman, Hany M. Fayed
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Publicado: Egyptian Society for Animal Management 2017
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Acceso en línea:https://dx.doi.org/10.21608/javs.2017.62129
https://doaj.org/article/dd3a664dfd5a44c1bdad00ec53c721de
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spelling oai:doaj.org-article:dd3a664dfd5a44c1bdad00ec53c721de2021-12-02T13:21:34ZPotential Therapeutic Role of Osteopontin Inhibition in Liver Fibrosis -Induced by Thioacetamide in Ratshttps://dx.doi.org/10.21608/javs.2017.621291687-40722090-3308https://doaj.org/article/dd3a664dfd5a44c1bdad00ec53c721de2017-10-01T00:00:00Zhttps://javs.journals.ekb.eg/article_62129.htmlhttps://doaj.org/toc/1687-4072https://doaj.org/toc/2090-3308To examine the effect of osteopontin inhibition by tranilast on liver fibrosis, four groups of rats were used throughout this study. Group I (Control group): rats received the solvent. Liver fibrosis was induced in Groups II, III, and IV by thioacetamide (TAA; 200mg/kg, ip) twice weekly for 6 weeks. Group II served as (TAA group). Groups III and IV (Treatment groups): rats were given tranilast for 6 weeks after TAA discontinuation. Liver osteopontin (OPN), transforming growth factor-β (TGF-β1), tumor necrosis factor alpha (TNF-α), alpha-smooth muscle actin (ɑ-SMA)), reduced glutathione (GSH), superoxide dismutase (SOD) and lipid peroxidation (MDA) were measured. Additionally, expression of α-smooth muscle actin (SMA) and caspase (Cas)-3 were assigned immunohistochemically. Treatment with tranilast prevented the development of hepatic fibrosis and the activation of stellate cells, and down-regulated the expression of genes for osteopontin and osteopontin-target molecules, including TGF-β and TNF-α and α-SMA.Tranilast significantly decreased MDA and increased levels of GSH, and SOD. Our findings suggest that targeting osteopontin with tranilast represents a new mode of therapy for liver fibrosis.Ramadan A.Nehal A. Afifi Nemat Z. Yassin Rehab F. Abdel-Rahman Sahar S. Abd El-RahmanHany M. Fayed Egyptian Society for Animal Managementarticleantioxidantapoptosisliver fibrosisosteopontinZoologyQL1-991Veterinary medicineSF600-1100Animal biochemistryQP501-801ENJournal of Applied Veterinary Sciences, Vol 2, Iss 1, Pp 1-8 (2017)
institution DOAJ
collection DOAJ
language EN
topic antioxidant
apoptosis
liver fibrosis
osteopontin
Zoology
QL1-991
Veterinary medicine
SF600-1100
Animal biochemistry
QP501-801
spellingShingle antioxidant
apoptosis
liver fibrosis
osteopontin
Zoology
QL1-991
Veterinary medicine
SF600-1100
Animal biochemistry
QP501-801
Ramadan A.
Nehal A. Afifi
Nemat Z. Yassin
Rehab F. Abdel-Rahman
Sahar S. Abd El-Rahman
Hany M. Fayed
Potential Therapeutic Role of Osteopontin Inhibition in Liver Fibrosis -Induced by Thioacetamide in Rats
description To examine the effect of osteopontin inhibition by tranilast on liver fibrosis, four groups of rats were used throughout this study. Group I (Control group): rats received the solvent. Liver fibrosis was induced in Groups II, III, and IV by thioacetamide (TAA; 200mg/kg, ip) twice weekly for 6 weeks. Group II served as (TAA group). Groups III and IV (Treatment groups): rats were given tranilast for 6 weeks after TAA discontinuation. Liver osteopontin (OPN), transforming growth factor-β (TGF-β1), tumor necrosis factor alpha (TNF-α), alpha-smooth muscle actin (ɑ-SMA)), reduced glutathione (GSH), superoxide dismutase (SOD) and lipid peroxidation (MDA) were measured. Additionally, expression of α-smooth muscle actin (SMA) and caspase (Cas)-3 were assigned immunohistochemically. Treatment with tranilast prevented the development of hepatic fibrosis and the activation of stellate cells, and down-regulated the expression of genes for osteopontin and osteopontin-target molecules, including TGF-β and TNF-α and α-SMA.Tranilast significantly decreased MDA and increased levels of GSH, and SOD. Our findings suggest that targeting osteopontin with tranilast represents a new mode of therapy for liver fibrosis.
format article
author Ramadan A.
Nehal A. Afifi
Nemat Z. Yassin
Rehab F. Abdel-Rahman
Sahar S. Abd El-Rahman
Hany M. Fayed
author_facet Ramadan A.
Nehal A. Afifi
Nemat Z. Yassin
Rehab F. Abdel-Rahman
Sahar S. Abd El-Rahman
Hany M. Fayed
author_sort Ramadan A.
title Potential Therapeutic Role of Osteopontin Inhibition in Liver Fibrosis -Induced by Thioacetamide in Rats
title_short Potential Therapeutic Role of Osteopontin Inhibition in Liver Fibrosis -Induced by Thioacetamide in Rats
title_full Potential Therapeutic Role of Osteopontin Inhibition in Liver Fibrosis -Induced by Thioacetamide in Rats
title_fullStr Potential Therapeutic Role of Osteopontin Inhibition in Liver Fibrosis -Induced by Thioacetamide in Rats
title_full_unstemmed Potential Therapeutic Role of Osteopontin Inhibition in Liver Fibrosis -Induced by Thioacetamide in Rats
title_sort potential therapeutic role of osteopontin inhibition in liver fibrosis -induced by thioacetamide in rats
publisher Egyptian Society for Animal Management
publishDate 2017
url https://dx.doi.org/10.21608/javs.2017.62129
https://doaj.org/article/dd3a664dfd5a44c1bdad00ec53c721de
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