Beneficial effects of benfotiamine, a NADPH oxidase inhibitor, in isoproterenol-induced myocardial infarction in rats
Acute myocardial infarction (AMI) remains the most common cause of morbidity and mortality worldwide. The present study was directed to investigate the beneficial effects of benfotiamine pre- and post-treatments in isoproterenol (ISO)-induced MI in rats. Myocardial heart damage was induced by subcut...
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description | Acute myocardial infarction (AMI) remains the most common cause of morbidity and mortality worldwide. The present study was directed to investigate the beneficial effects of benfotiamine pre- and post-treatments in isoproterenol (ISO)-induced MI in rats.
Myocardial heart damage was induced by subcutaneous injection of ISO (150 mg/kg) once daily for two consecutive days. Benfotiamine (100 mg/kg/day) was given orally for two weeks before or after ISO treatment.
ISO administration revealed significant changes in electrocardiographic recordings, elevation of levels of cardiac enzymes; creatinine kinase (CK-MB) and troponin-I (cTn-I), and perturbation of markers of oxidative stress; nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD) and glutathione peroxidase (GPx) and markers of inflammation; protein kinase C (PKC), nuclear factor-kappa B (NF-κB) and metalloproteinase-9 (MMP-9). The apoptotic markers (caspase-8 and p53) were also significantly elevated in ISO groups in addition to histological alterations. Groups treated with benfotiamine pre- and post-ISO administration showed significantly decreased cardiac enzymes levels and improved oxidative stress, inflammatory and apoptotic markers compared to the ISO groups.
The current study highlights the potential role of benfotiamine as a promising agent for prophylactic and therapeutic interventions in myocardial damage in several cardiovascular disorders via NADPH oxidase inhibition. |
doi_str_mv | 10.1371/journal.pone.0232413 |
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Myocardial heart damage was induced by subcutaneous injection of ISO (150 mg/kg) once daily for two consecutive days. Benfotiamine (100 mg/kg/day) was given orally for two weeks before or after ISO treatment.
ISO administration revealed significant changes in electrocardiographic recordings, elevation of levels of cardiac enzymes; creatinine kinase (CK-MB) and troponin-I (cTn-I), and perturbation of markers of oxidative stress; nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD) and glutathione peroxidase (GPx) and markers of inflammation; protein kinase C (PKC), nuclear factor-kappa B (NF-κB) and metalloproteinase-9 (MMP-9). The apoptotic markers (caspase-8 and p53) were also significantly elevated in ISO groups in addition to histological alterations. Groups treated with benfotiamine pre- and post-ISO administration showed significantly decreased cardiac enzymes levels and improved oxidative stress, inflammatory and apoptotic markers compared to the ISO groups.
The current study highlights the potential role of benfotiamine as a promising agent for prophylactic and therapeutic interventions in myocardial damage in several cardiovascular disorders via NADPH oxidase inhibition.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0232413</identifier><identifier>PMID: 32384080</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adenine ; Apoptosis ; Biology and Life Sciences ; Calcium-binding protein ; Cardiomyocytes ; Caspase-8 ; Chemical compounds ; Creatine kinase ; Creatinine ; Damage ; Diabetes ; Drug therapy ; Electrocardiography ; Enzyme inhibitors ; Enzymes ; Gelatinase B ; Glutathione ; Glutathione peroxidase ; Health aspects ; Heart ; Heart attack ; Heart attacks ; Inflammation ; Isoproterenol ; Kinases ; Laboratory animals ; Malondialdehyde ; Markers ; Medicine and Health Sciences ; Membrane proteins ; Metalloproteinase ; Morbidity ; Myocardial infarction ; NAD(P)H oxidase ; NADPH-diaphorase ; NF-κB protein ; Niacinamide ; Nicotinamide ; Nicotinamide adenine dinucleotide ; Oxidase ; Oxidases ; Oxidative stress ; p53 Protein ; Peroxidase ; Perturbation ; Pharmacology ; Pharmacy ; Phosphates ; Protein kinase C ; Protein kinases ; Proteins ; Purines ; Research and Analysis Methods ; Superoxide dismutase ; Superoxides ; Testing ; Therapeutic applications ; Toxicology ; Troponin ; Tumor proteins ; Vitamin B</subject><ispartof>PloS one, 2020-05, Vol.15 (5), p.e0232413</ispartof><rights>COPYRIGHT 2020 Public Library of Science</rights><rights>2020 Ahmed et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020 Ahmed et al 2020 Ahmed et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-e4b118fe32a357ab7ec75cf35a4255bd5986073b7661a30a425a18adce364de53</citedby><cites>FETCH-LOGICAL-c692t-e4b118fe32a357ab7ec75cf35a4255bd5986073b7661a30a425a18adce364de53</cites><orcidid>0000-0003-3476-2815</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7209119/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7209119/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53769,53771,79346,79347</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32384080$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Bader, Michael</contributor><creatorcontrib>Ahmed, Lamiaa A</creatorcontrib><creatorcontrib>Hassan, Omnia F</creatorcontrib><creatorcontrib>Galal, Omneya</creatorcontrib><creatorcontrib>Mansour, Dina F</creatorcontrib><creatorcontrib>El-Khatib, Aiman</creatorcontrib><title>Beneficial effects of benfotiamine, a NADPH oxidase inhibitor, in isoproterenol-induced myocardial infarction in rats</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Acute myocardial infarction (AMI) remains the most common cause of morbidity and mortality worldwide. The present study was directed to investigate the beneficial effects of benfotiamine pre- and post-treatments in isoproterenol (ISO)-induced MI in rats.
Myocardial heart damage was induced by subcutaneous injection of ISO (150 mg/kg) once daily for two consecutive days. Benfotiamine (100 mg/kg/day) was given orally for two weeks before or after ISO treatment.
ISO administration revealed significant changes in electrocardiographic recordings, elevation of levels of cardiac enzymes; creatinine kinase (CK-MB) and troponin-I (cTn-I), and perturbation of markers of oxidative stress; nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD) and glutathione peroxidase (GPx) and markers of inflammation; protein kinase C (PKC), nuclear factor-kappa B (NF-κB) and metalloproteinase-9 (MMP-9). The apoptotic markers (caspase-8 and p53) were also significantly elevated in ISO groups in addition to histological alterations. Groups treated with benfotiamine pre- and post-ISO administration showed significantly decreased cardiac enzymes levels and improved oxidative stress, inflammatory and apoptotic markers compared to the ISO groups.
The current study highlights the potential role of benfotiamine as a promising agent for prophylactic and therapeutic interventions in myocardial damage in several cardiovascular disorders via NADPH oxidase inhibition.</description><subject>Adenine</subject><subject>Apoptosis</subject><subject>Biology and Life Sciences</subject><subject>Calcium-binding protein</subject><subject>Cardiomyocytes</subject><subject>Caspase-8</subject><subject>Chemical compounds</subject><subject>Creatine kinase</subject><subject>Creatinine</subject><subject>Damage</subject><subject>Diabetes</subject><subject>Drug therapy</subject><subject>Electrocardiography</subject><subject>Enzyme inhibitors</subject><subject>Enzymes</subject><subject>Gelatinase B</subject><subject>Glutathione</subject><subject>Glutathione peroxidase</subject><subject>Health aspects</subject><subject>Heart</subject><subject>Heart attack</subject><subject>Heart attacks</subject><subject>Inflammation</subject><subject>Isoproterenol</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Malondialdehyde</subject><subject>Markers</subject><subject>Medicine and Health Sciences</subject><subject>Membrane proteins</subject><subject>Metalloproteinase</subject><subject>Morbidity</subject><subject>Myocardial infarction</subject><subject>NAD(P)H oxidase</subject><subject>NADPH-diaphorase</subject><subject>NF-κB protein</subject><subject>Niacinamide</subject><subject>Nicotinamide</subject><subject>Nicotinamide adenine dinucleotide</subject><subject>Oxidase</subject><subject>Oxidases</subject><subject>Oxidative stress</subject><subject>p53 Protein</subject><subject>Peroxidase</subject><subject>Perturbation</subject><subject>Pharmacology</subject><subject>Pharmacy</subject><subject>Phosphates</subject><subject>Protein kinase C</subject><subject>Protein kinases</subject><subject>Proteins</subject><subject>Purines</subject><subject>Research and Analysis Methods</subject><subject>Superoxide dismutase</subject><subject>Superoxides</subject><subject>Testing</subject><subject>Therapeutic applications</subject><subject>Toxicology</subject><subject>Troponin</subject><subject>Tumor proteins</subject><subject>Vitamin 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effects of benfotiamine, a NADPH oxidase inhibitor, in isoproterenol-induced myocardial infarction in rats</title><author>Ahmed, Lamiaa A ; Hassan, Omnia F ; Galal, Omneya ; Mansour, Dina F ; El-Khatib, Aiman</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-e4b118fe32a357ab7ec75cf35a4255bd5986073b7661a30a425a18adce364de53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adenine</topic><topic>Apoptosis</topic><topic>Biology and Life Sciences</topic><topic>Calcium-binding protein</topic><topic>Cardiomyocytes</topic><topic>Caspase-8</topic><topic>Chemical compounds</topic><topic>Creatine kinase</topic><topic>Creatinine</topic><topic>Damage</topic><topic>Diabetes</topic><topic>Drug therapy</topic><topic>Electrocardiography</topic><topic>Enzyme inhibitors</topic><topic>Enzymes</topic><topic>Gelatinase B</topic><topic>Glutathione</topic><topic>Glutathione peroxidase</topic><topic>Health aspects</topic><topic>Heart</topic><topic>Heart attack</topic><topic>Heart attacks</topic><topic>Inflammation</topic><topic>Isoproterenol</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Malondialdehyde</topic><topic>Markers</topic><topic>Medicine and Health Sciences</topic><topic>Membrane proteins</topic><topic>Metalloproteinase</topic><topic>Morbidity</topic><topic>Myocardial infarction</topic><topic>NAD(P)H oxidase</topic><topic>NADPH-diaphorase</topic><topic>NF-κB protein</topic><topic>Niacinamide</topic><topic>Nicotinamide</topic><topic>Nicotinamide adenine dinucleotide</topic><topic>Oxidase</topic><topic>Oxidases</topic><topic>Oxidative stress</topic><topic>p53 Protein</topic><topic>Peroxidase</topic><topic>Perturbation</topic><topic>Pharmacology</topic><topic>Pharmacy</topic><topic>Phosphates</topic><topic>Protein kinase C</topic><topic>Protein kinases</topic><topic>Proteins</topic><topic>Purines</topic><topic>Research and 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Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ahmed, Lamiaa A</au><au>Hassan, Omnia F</au><au>Galal, Omneya</au><au>Mansour, Dina F</au><au>El-Khatib, Aiman</au><au>Bader, Michael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Beneficial effects of benfotiamine, a NADPH oxidase inhibitor, in isoproterenol-induced myocardial infarction in rats</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2020-05-08</date><risdate>2020</risdate><volume>15</volume><issue>5</issue><spage>e0232413</spage><pages>e0232413-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Acute myocardial infarction (AMI) remains the most common cause of morbidity and mortality worldwide. The present study was directed to investigate the beneficial effects of benfotiamine pre- and post-treatments in isoproterenol (ISO)-induced MI in rats.
Myocardial heart damage was induced by subcutaneous injection of ISO (150 mg/kg) once daily for two consecutive days. Benfotiamine (100 mg/kg/day) was given orally for two weeks before or after ISO treatment.
ISO administration revealed significant changes in electrocardiographic recordings, elevation of levels of cardiac enzymes; creatinine kinase (CK-MB) and troponin-I (cTn-I), and perturbation of markers of oxidative stress; nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD) and glutathione peroxidase (GPx) and markers of inflammation; protein kinase C (PKC), nuclear factor-kappa B (NF-κB) and metalloproteinase-9 (MMP-9). The apoptotic markers (caspase-8 and p53) were also significantly elevated in ISO groups in addition to histological alterations. Groups treated with benfotiamine pre- and post-ISO administration showed significantly decreased cardiac enzymes levels and improved oxidative stress, inflammatory and apoptotic markers compared to the ISO groups.
The current study highlights the potential role of benfotiamine as a promising agent for prophylactic and therapeutic interventions in myocardial damage in several cardiovascular disorders via NADPH oxidase inhibition.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>32384080</pmid><doi>10.1371/journal.pone.0232413</doi><tpages>e0232413</tpages><orcidid>https://orcid.org/0000-0003-3476-2815</orcidid><oa>free_for_read</oa></addata></record> |
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source | DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
subjects | Adenine Apoptosis Biology and Life Sciences Calcium-binding protein Cardiomyocytes Caspase-8 Chemical compounds Creatine kinase Creatinine Damage Diabetes Drug therapy Electrocardiography Enzyme inhibitors Enzymes Gelatinase B Glutathione Glutathione peroxidase Health aspects Heart Heart attack Heart attacks Inflammation Isoproterenol Kinases Laboratory animals Malondialdehyde Markers Medicine and Health Sciences Membrane proteins Metalloproteinase Morbidity Myocardial infarction NAD(P)H oxidase NADPH-diaphorase NF-κB protein Niacinamide Nicotinamide Nicotinamide adenine dinucleotide Oxidase Oxidases Oxidative stress p53 Protein Peroxidase Perturbation Pharmacology Pharmacy Phosphates Protein kinase C Protein kinases Proteins Purines Research and Analysis Methods Superoxide dismutase Superoxides Testing Therapeutic applications Toxicology Troponin Tumor proteins Vitamin B |
title | Beneficial effects of benfotiamine, a NADPH oxidase inhibitor, in isoproterenol-induced myocardial infarction in rats |
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