The protective potential of alpha lipoic acid on amiodarone-induced pulmonary fibrosis and hepatic injury in rats
Amiodarone (AMD) is a widely used antiarrhythmic drug prescribed to treat cardiac tachyarrhythmias; however, AMD has been reported to provoke pulmonary fibrosis (PF) and hepatotoxicity. This study aimed to investigate the influence of alpha lipoic acid (ALA) on AMD-induced PF and hepatotoxicity in m...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2021-09, Vol.476 (9), p.3433-3448 |
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| description | Amiodarone (AMD) is a widely used antiarrhythmic drug prescribed to treat cardiac tachyarrhythmias; however, AMD has been reported to provoke pulmonary fibrosis (PF) and hepatotoxicity. This study aimed to investigate the influence of alpha lipoic acid (ALA) on AMD-induced PF and hepatotoxicity in male Wistar rats. AMD administration resulted in elevated lung contents of hydroxyproline (Hyp), malondialdehyde (MDA), and increased serum levels of transforming growth factor beta-1 (TGF-β1), interferon-γ (IFN-γ), alanine amino transaminase (ALT), aspartate amino transaminase (AST), total cholesterol (TC), and glucose. On the other side, lung content of glutathione reduced (GSH) and serum levels of total anti-oxidant capacity (TAC) were significantly decreased. Histopathologically, AMD caused PF, produced a mild hepatic injury, and increased expression of alpha smooth muscle actin (α-SMA). Treatment with ALA produced a significant reversal of the oxidative stress, fibrosis, and inflammation parameters with reductions in α-SMA expressions, leading to amelioration of histopathological lesions. ALA might provide supportive therapy in AMD-receiving cardiovascular patients. |
| doi_str_mv | 10.1007/s11010-021-04173-7 |
| format | Article |
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Mousa, Mohamed</creator><creatorcontrib>Ibrahim Fouad, Ghadha ; R. Mousa, Mohamed</creatorcontrib><description>Amiodarone (AMD) is a widely used antiarrhythmic drug prescribed to treat cardiac tachyarrhythmias; however, AMD has been reported to provoke pulmonary fibrosis (PF) and hepatotoxicity. This study aimed to investigate the influence of alpha lipoic acid (ALA) on AMD-induced PF and hepatotoxicity in male Wistar rats. AMD administration resulted in elevated lung contents of hydroxyproline (Hyp), malondialdehyde (MDA), and increased serum levels of transforming growth factor beta-1 (TGF-β1), interferon-γ (IFN-γ), alanine amino transaminase (ALT), aspartate amino transaminase (AST), total cholesterol (TC), and glucose. On the other side, lung content of glutathione reduced (GSH) and serum levels of total anti-oxidant capacity (TAC) were significantly decreased. Histopathologically, AMD caused PF, produced a mild hepatic injury, and increased expression of alpha smooth muscle actin (α-SMA). Treatment with ALA produced a significant reversal of the oxidative stress, fibrosis, and inflammation parameters with reductions in α-SMA expressions, leading to amelioration of histopathological lesions. ALA might provide supportive therapy in AMD-receiving cardiovascular patients.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-021-04173-7</identifier><identifier>PMID: 33973131</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Actin ; Alanine ; Amiodarone ; Antioxidants ; Aspartate ; Biochemistry ; Biological response modifiers ; Biomedical and Life Sciences ; Cardiology ; Cholesterol ; Fibrosis ; Glutathione ; Growth factors ; Hepatotoxicity ; Hydroxyproline ; Inflammation ; Interferon ; Life Sciences ; Lipoic acid ; Liver ; Lung diseases ; Lungs ; Malondialdehyde ; Medical Biochemistry ; Muscle proteins ; Muscles ; Oncology ; Oxidants ; Oxidative stress ; Oxidizing agents ; Pulmonary fibrosis ; Rodents ; Serum levels ; Smooth muscle ; Transaminase ; Transaminases ; Transforming growth factor-b1 ; Transforming growth factors ; γ-Interferon</subject><ispartof>Molecular and cellular biochemistry, 2021-09, Vol.476 (9), p.3433-3448</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>COPYRIGHT 2021 Springer</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-429701ba042be7557bd698fc8ce5184e6c7aa4e9b6e5ea894e185ddfc6a90d543</citedby><cites>FETCH-LOGICAL-c442t-429701ba042be7557bd698fc8ce5184e6c7aa4e9b6e5ea894e185ddfc6a90d543</cites><orcidid>0000-0003-3665-3153</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-021-04173-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-021-04173-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27926,27927,41490,42559,51321</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33973131$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ibrahim Fouad, Ghadha</creatorcontrib><creatorcontrib>R. Mousa, Mohamed</creatorcontrib><title>The protective potential of alpha lipoic acid on amiodarone-induced pulmonary fibrosis and hepatic injury in rats</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>Amiodarone (AMD) is a widely used antiarrhythmic drug prescribed to treat cardiac tachyarrhythmias; however, AMD has been reported to provoke pulmonary fibrosis (PF) and hepatotoxicity. This study aimed to investigate the influence of alpha lipoic acid (ALA) on AMD-induced PF and hepatotoxicity in male Wistar rats. AMD administration resulted in elevated lung contents of hydroxyproline (Hyp), malondialdehyde (MDA), and increased serum levels of transforming growth factor beta-1 (TGF-β1), interferon-γ (IFN-γ), alanine amino transaminase (ALT), aspartate amino transaminase (AST), total cholesterol (TC), and glucose. On the other side, lung content of glutathione reduced (GSH) and serum levels of total anti-oxidant capacity (TAC) were significantly decreased. Histopathologically, AMD caused PF, produced a mild hepatic injury, and increased expression of alpha smooth muscle actin (α-SMA). Treatment with ALA produced a significant reversal of the oxidative stress, fibrosis, and inflammation parameters with reductions in α-SMA expressions, leading to amelioration of histopathological lesions. ALA might provide supportive therapy in AMD-receiving cardiovascular patients.</description><subject>Actin</subject><subject>Alanine</subject><subject>Amiodarone</subject><subject>Antioxidants</subject><subject>Aspartate</subject><subject>Biochemistry</subject><subject>Biological response modifiers</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiology</subject><subject>Cholesterol</subject><subject>Fibrosis</subject><subject>Glutathione</subject><subject>Growth factors</subject><subject>Hepatotoxicity</subject><subject>Hydroxyproline</subject><subject>Inflammation</subject><subject>Interferon</subject><subject>Life Sciences</subject><subject>Lipoic acid</subject><subject>Liver</subject><subject>Lung diseases</subject><subject>Lungs</subject><subject>Malondialdehyde</subject><subject>Medical Biochemistry</subject><subject>Muscle proteins</subject><subject>Muscles</subject><subject>Oncology</subject><subject>Oxidants</subject><subject>Oxidative stress</subject><subject>Oxidizing agents</subject><subject>Pulmonary fibrosis</subject><subject>Rodents</subject><subject>Serum levels</subject><subject>Smooth muscle</subject><subject>Transaminase</subject><subject>Transaminases</subject><subject>Transforming growth factor-b1</subject><subject>Transforming growth factors</subject><subject>γ-Interferon</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9UcFu1TAQtBCIvhZ-gAOyxDnFG9txfKwqCpUqcSlny7E3fX5K7NROkPh7_HiFCgkhH7zyzox3Zwh5B-wSGFMfCwAD1rAWGiZA8Ua9IDuQtRAa9EuyY5yxpgelzsh5KQdW0QzgNTnjXCsOHHbk8X6PdMlpRbeG77WsVVyDnWgaqZ2WvaVTWFJw1LrgaYrUziF5m1PEJkS_OfR02aY5RZt_0DEMOZVQqI2e7nGxa2WGeNhqL0Sa7VrekFejnQq-fbovyLebT_fXX5q7r59vr6_uGidEuzai1YrBYJloB1RSqsF3uh9d71BCL7BzylqBeuhQou21QOil96PrrGZeCn5BPpx063aPG5bVHNKWY_3StFL2rYLqzDPqwU5oQhzTmq2bQ3HmqlNMK8X5UevyH6h6PM7BVSvGUN__IrQngqt2lIyjWXKYq0MGmDmGZ07hmRqe-RWeOc7y_mnibZjR_6H8TqsC-AlQais-YH5e6T-yPwEtpaSg</recordid><startdate>20210901</startdate><enddate>20210901</enddate><creator>Ibrahim Fouad, Ghadha</creator><creator>R. 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Mousa, Mohamed</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-429701ba042be7557bd698fc8ce5184e6c7aa4e9b6e5ea894e185ddfc6a90d543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Actin</topic><topic>Alanine</topic><topic>Amiodarone</topic><topic>Antioxidants</topic><topic>Aspartate</topic><topic>Biochemistry</topic><topic>Biological response modifiers</topic><topic>Biomedical and Life Sciences</topic><topic>Cardiology</topic><topic>Cholesterol</topic><topic>Fibrosis</topic><topic>Glutathione</topic><topic>Growth factors</topic><topic>Hepatotoxicity</topic><topic>Hydroxyproline</topic><topic>Inflammation</topic><topic>Interferon</topic><topic>Life Sciences</topic><topic>Lipoic acid</topic><topic>Liver</topic><topic>Lung diseases</topic><topic>Lungs</topic><topic>Malondialdehyde</topic><topic>Medical Biochemistry</topic><topic>Muscle proteins</topic><topic>Muscles</topic><topic>Oncology</topic><topic>Oxidants</topic><topic>Oxidative stress</topic><topic>Oxidizing agents</topic><topic>Pulmonary fibrosis</topic><topic>Rodents</topic><topic>Serum levels</topic><topic>Smooth muscle</topic><topic>Transaminase</topic><topic>Transaminases</topic><topic>Transforming growth factor-b1</topic><topic>Transforming growth factors</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ibrahim Fouad, Ghadha</creatorcontrib><creatorcontrib>R. 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Mousa, Mohamed</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The protective potential of alpha lipoic acid on amiodarone-induced pulmonary fibrosis and hepatic injury in rats</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2021-09-01</date><risdate>2021</risdate><volume>476</volume><issue>9</issue><spage>3433</spage><epage>3448</epage><pages>3433-3448</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Amiodarone (AMD) is a widely used antiarrhythmic drug prescribed to treat cardiac tachyarrhythmias; however, AMD has been reported to provoke pulmonary fibrosis (PF) and hepatotoxicity. This study aimed to investigate the influence of alpha lipoic acid (ALA) on AMD-induced PF and hepatotoxicity in male Wistar rats. AMD administration resulted in elevated lung contents of hydroxyproline (Hyp), malondialdehyde (MDA), and increased serum levels of transforming growth factor beta-1 (TGF-β1), interferon-γ (IFN-γ), alanine amino transaminase (ALT), aspartate amino transaminase (AST), total cholesterol (TC), and glucose. On the other side, lung content of glutathione reduced (GSH) and serum levels of total anti-oxidant capacity (TAC) were significantly decreased. Histopathologically, AMD caused PF, produced a mild hepatic injury, and increased expression of alpha smooth muscle actin (α-SMA). Treatment with ALA produced a significant reversal of the oxidative stress, fibrosis, and inflammation parameters with reductions in α-SMA expressions, leading to amelioration of histopathological lesions. ALA might provide supportive therapy in AMD-receiving cardiovascular patients.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>33973131</pmid><doi>10.1007/s11010-021-04173-7</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0003-3665-3153</orcidid></addata></record> |
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| subjects | Actin Alanine Amiodarone Antioxidants Aspartate Biochemistry Biological response modifiers Biomedical and Life Sciences Cardiology Cholesterol Fibrosis Glutathione Growth factors Hepatotoxicity Hydroxyproline Inflammation Interferon Life Sciences Lipoic acid Liver Lung diseases Lungs Malondialdehyde Medical Biochemistry Muscle proteins Muscles Oncology Oxidants Oxidative stress Oxidizing agents Pulmonary fibrosis Rodents Serum levels Smooth muscle Transaminase Transaminases Transforming growth factor-b1 Transforming growth factors γ-Interferon |
| title | The protective potential of alpha lipoic acid on amiodarone-induced pulmonary fibrosis and hepatic injury in rats |
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