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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Veröffentlicht in:PloS one 2020-05, Vol.15 (5), p.e0232413
Hauptverfasser: Ahmed, Lamiaa A, Hassan, Omnia F, Galal, Omneya, Mansour, Dina F, El-Khatib, Aiman
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Galal, Omneya
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El-Khatib, Aiman
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.
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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. 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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). 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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 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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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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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