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Metformin attenuates oxidative stress and liver damage after bile duct ligation in rats

The aim of the current study was to investigate the antioxidative effect of metformin (MTF) on bile duct ligation (BDL)-induced hepatic disorder and histological damage in rats. The rats were divided into 4 groups including sham control (SC), BDL alone (BDL surgery), MTF1 (BDL surgery and administra...

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Autores principales: Sadeghi, Heibatollah, Jahanbazi, Fatemeh, Sadeghi, Hossein, Omidifar, Navid, Alipoor, Behnam, Kokhdan, Esmaeel Panahi, Mousavipoor, Seyed Mehdi, Mousavi-Fard, Seyed Hossein, Doustimotlagh, Amir Hossein
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer - Medknow 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6791170/
https://www.ncbi.nlm.nih.gov/pubmed/31620188
http://dx.doi.org/10.4103/1735-5362.253359
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author Sadeghi, Heibatollah
Jahanbazi, Fatemeh
Sadeghi, Hossein
Omidifar, Navid
Alipoor, Behnam
Kokhdan, Esmaeel Panahi
Mousavipoor, Seyed Mehdi
Mousavi-Fard, Seyed Hossein
Doustimotlagh, Amir Hossein
author_facet Sadeghi, Heibatollah
Jahanbazi, Fatemeh
Sadeghi, Hossein
Omidifar, Navid
Alipoor, Behnam
Kokhdan, Esmaeel Panahi
Mousavipoor, Seyed Mehdi
Mousavi-Fard, Seyed Hossein
Doustimotlagh, Amir Hossein
author_sort Sadeghi, Heibatollah
collection PubMed
description The aim of the current study was to investigate the antioxidative effect of metformin (MTF) on bile duct ligation (BDL)-induced hepatic disorder and histological damage in rats. The rats were divided into 4 groups including sham control (SC), BDL alone (BDL surgery), MTF1 (BDL surgery and administration of 250 mg/kg of MFM) and MTF2 (BDL surgery and administration of 500 mg/kg of MTF). After BDL, the animals treated with MTF by gavage for 10 days. Hematoxylin and eosin staining, biochemical analysis and oxidative stress markers were assayed to determine histological alterations, liver functions, and oxidant/antioxidant status. Hepatotoxicity was verified by remarkable increase in plasma levels of aminotransferases and alkaline phosphatase activity and liver histology 10 days after the BDL surgery. Our finding showed that treatment with MTF markedly reduced plasma alkaline phosphatase and alleviated liver injury indices (P ≤ 0.05). Furthermore, BDL caused a considerable increase in the protein carbonyl and malondialdehyde content (P ≤ 0.05). However, MTF reduces oxidative stress by constraining the protein oxidation and lipid peroxidation, and increases antioxidant reserve by increasing the ferric reducing ability of plasma and reducing glutathione levels. MTF exerts antioxidative effects in the liver fibrosis and may represent a hepato-protective effect when given to rats with BDL-induced hepatic injury.
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spelling pubmed-67911702019-10-16 Metformin attenuates oxidative stress and liver damage after bile duct ligation in rats Sadeghi, Heibatollah Jahanbazi, Fatemeh Sadeghi, Hossein Omidifar, Navid Alipoor, Behnam Kokhdan, Esmaeel Panahi Mousavipoor, Seyed Mehdi Mousavi-Fard, Seyed Hossein Doustimotlagh, Amir Hossein Res Pharm Sci Original Article The aim of the current study was to investigate the antioxidative effect of metformin (MTF) on bile duct ligation (BDL)-induced hepatic disorder and histological damage in rats. The rats were divided into 4 groups including sham control (SC), BDL alone (BDL surgery), MTF1 (BDL surgery and administration of 250 mg/kg of MFM) and MTF2 (BDL surgery and administration of 500 mg/kg of MTF). After BDL, the animals treated with MTF by gavage for 10 days. Hematoxylin and eosin staining, biochemical analysis and oxidative stress markers were assayed to determine histological alterations, liver functions, and oxidant/antioxidant status. Hepatotoxicity was verified by remarkable increase in plasma levels of aminotransferases and alkaline phosphatase activity and liver histology 10 days after the BDL surgery. Our finding showed that treatment with MTF markedly reduced plasma alkaline phosphatase and alleviated liver injury indices (P ≤ 0.05). Furthermore, BDL caused a considerable increase in the protein carbonyl and malondialdehyde content (P ≤ 0.05). However, MTF reduces oxidative stress by constraining the protein oxidation and lipid peroxidation, and increases antioxidant reserve by increasing the ferric reducing ability of plasma and reducing glutathione levels. MTF exerts antioxidative effects in the liver fibrosis and may represent a hepato-protective effect when given to rats with BDL-induced hepatic injury. Wolters Kluwer - Medknow 2019-03-08 /pmc/articles/PMC6791170/ /pubmed/31620188 http://dx.doi.org/10.4103/1735-5362.253359 Text en Copyright: © 2019 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
Sadeghi, Heibatollah
Jahanbazi, Fatemeh
Sadeghi, Hossein
Omidifar, Navid
Alipoor, Behnam
Kokhdan, Esmaeel Panahi
Mousavipoor, Seyed Mehdi
Mousavi-Fard, Seyed Hossein
Doustimotlagh, Amir Hossein
Metformin attenuates oxidative stress and liver damage after bile duct ligation in rats
title Metformin attenuates oxidative stress and liver damage after bile duct ligation in rats
title_full Metformin attenuates oxidative stress and liver damage after bile duct ligation in rats
title_fullStr Metformin attenuates oxidative stress and liver damage after bile duct ligation in rats
title_full_unstemmed Metformin attenuates oxidative stress and liver damage after bile duct ligation in rats
title_short Metformin attenuates oxidative stress and liver damage after bile duct ligation in rats
title_sort metformin attenuates oxidative stress and liver damage after bile duct ligation in rats
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6791170/
https://www.ncbi.nlm.nih.gov/pubmed/31620188
http://dx.doi.org/10.4103/1735-5362.253359
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