(E)-N′-(1-(7-Hydroxy-2-Oxo-2H-Chromen-3-Yl) Ethylidene) Benzohydrazide, a Novel Synthesized Coumarin, Ameliorates Isoproterenol-Induced Myocardial Infarction in Rats through Attenuating Oxidative Stress, Inflammation, and Apoptosis
The present study was directed to investigate the effect of precotreatment with (E)-N′-(1-(7-hydroxy-2-oxo-2H-chromen-3-yl) ethylidene) benzohydrazide (7-hyd.HC), a novel potent synthesized coumarin, on isoproterenol- (ISO-) induced myocardial infarction (MI) in rats. The hydrazone compound was char...
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| Vydané v: | Oxidative medicine and cellular longevity Ročník 2020; číslo 2020; s. 1 - 15 |
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| Hlavní autori: | , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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Cairo, Egypt
Hindawi Publishing Corporation
2020
Hindawi John Wiley & Sons, Inc |
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| ISSN: | 1942-0900, 1942-0994, 1942-0994 |
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| Abstract | The present study was directed to investigate the effect of precotreatment with (E)-N′-(1-(7-hydroxy-2-oxo-2H-chromen-3-yl) ethylidene) benzohydrazide (7-hyd.HC), a novel potent synthesized coumarin, on isoproterenol- (ISO-) induced myocardial infarction (MI) in rats. The hydrazone compound was characterized by IR, 1D, and 2D NMR analyses. Experimental induction of MI in rats was established by ISO (85 mg/kg/day, s.c) for two consecutive days (6th and 7th days). 7-hyd.HC or sintrom was given for 7 days prior and simultaneous to ISO injection. 7-hyd.HC offered a cardiopreventive effect by preventing heart injury marker leakage (LDH, ALT, AST, CK-MB, and cTn-I) from cardiomyocytes and normalizing cardiac function and ECG pattern, as well as improving lipid profile (TC, TG, LDL-C, and HDL-C), which were altered by ISO administration. Moreover, 7-hyd.HC precotreatment significantly mitigated the oxidative stress biomarkers, as evidenced by the decrease of lipid peroxidation and the increased level of the myocardial GSH level together with the SOD, GSH-Px, and catalase activities. 7-hyd.HC inhibited the cardiac apoptosis by upregulating the expression of Bcl-2 and downregulating the expression of Bax and caspase-3 genes. In addition, 7-hyd.HC reduced the elevated fibrinogen rate and better prevented the myocardial necrosis and improved the interstitial edema and neutrophil infiltration than sintrom. Overall, 7-hyd.HC ameliorated the severity of ISO-induced myocardial infarction through improving the oxidative status, attenuating apoptosis, and reducing fibrinogen production. The 7-hyd.HC actions could be mediated by its antioxidant, antiapoptotic, and anti-inflammatory capacities. |
|---|---|
| AbstractList | The present study was directed to investigate the effect of precotreatment with (E)-N'-(1-(7-hydroxy-2-oxo-2H-chromen-3-yl) ethylidene) benzohydrazide (7-hyd.HC), a novel potent synthesized coumarin, on isoproterenol- (ISO-) induced myocardial infarction (MI) in rats. The hydrazone compound was characterized by IR, 1D, and 2D NMR analyses. Experimental induction of MI in rats was established by ISO (85 mg/kg/day, s.c) for two consecutive days (6th and 7th days). 7-hyd.HC or sintrom was given for 7 days prior and simultaneous to ISO injection. 7-hyd.HC offered a cardiopreventive effect by preventing heart injury marker leakage (LDH, ALT, AST, CK-MB, and cTn-I) from cardiomyocytes and normalizing cardiac function and ECG pattern, as well as improving lipid profile (TC, TG, LDL-C, and HDL-C), which were altered by ISO administration. Moreover, 7-hyd.HC precotreatment significantly mitigated the oxidative stress biomarkers, as evidenced by the decrease of lipid peroxidation and the increased level of the myocardial GSH level together with the SOD, GSH-Px, and catalase activities. 7-hyd.HC inhibited the cardiac apoptosis by upregulating the expression of Bcl-2 and downregulating the expression of Bax and caspase-3 genes. In addition, 7-hyd.HC reduced the elevated fibrinogen rate and better prevented the myocardial necrosis and improved the interstitial edema and neutrophil infiltration than sintrom. Overall, 7-hyd.HC ameliorated the severity of ISO-induced myocardial infarction through improving the oxidative status, attenuating apoptosis, and reducing fibrinogen production. The 7-hyd.HC actions could be mediated by its antioxidant, antiapoptotic, and anti-inflammatory capacities.The present study was directed to investigate the effect of precotreatment with (E)-N'-(1-(7-hydroxy-2-oxo-2H-chromen-3-yl) ethylidene) benzohydrazide (7-hyd.HC), a novel potent synthesized coumarin, on isoproterenol- (ISO-) induced myocardial infarction (MI) in rats. The hydrazone compound was characterized by IR, 1D, and 2D NMR analyses. Experimental induction of MI in rats was established by ISO (85 mg/kg/day, s.c) for two consecutive days (6th and 7th days). 7-hyd.HC or sintrom was given for 7 days prior and simultaneous to ISO injection. 7-hyd.HC offered a cardiopreventive effect by preventing heart injury marker leakage (LDH, ALT, AST, CK-MB, and cTn-I) from cardiomyocytes and normalizing cardiac function and ECG pattern, as well as improving lipid profile (TC, TG, LDL-C, and HDL-C), which were altered by ISO administration. Moreover, 7-hyd.HC precotreatment significantly mitigated the oxidative stress biomarkers, as evidenced by the decrease of lipid peroxidation and the increased level of the myocardial GSH level together with the SOD, GSH-Px, and catalase activities. 7-hyd.HC inhibited the cardiac apoptosis by upregulating the expression of Bcl-2 and downregulating the expression of Bax and caspase-3 genes. In addition, 7-hyd.HC reduced the elevated fibrinogen rate and better prevented the myocardial necrosis and improved the interstitial edema and neutrophil infiltration than sintrom. Overall, 7-hyd.HC ameliorated the severity of ISO-induced myocardial infarction through improving the oxidative status, attenuating apoptosis, and reducing fibrinogen production. The 7-hyd.HC actions could be mediated by its antioxidant, antiapoptotic, and anti-inflammatory capacities. The present study was directed to investigate the effect of precotreatment with (E)-N′-(1-(7-hydroxy-2-oxo-2H-chromen-3-yl) ethylidene) benzohydrazide (7-hyd.HC), a novel potent synthesized coumarin, on isoproterenol- (ISO-) induced myocardial infarction (MI) in rats. The hydrazone compound was characterized by IR, 1D, and 2D NMR analyses. Experimental induction of MI in rats was established by ISO (85 mg/kg/day, s.c) for two consecutive days (6th and 7th days). 7-hyd.HC or sintrom was given for 7 days prior and simultaneous to ISO injection. 7-hyd.HC offered a cardiopreventive effect by preventing heart injury marker leakage (LDH, ALT, AST, CK-MB, and cTn-I) from cardiomyocytes and normalizing cardiac function and ECG pattern, as well as improving lipid profile (TC, TG, LDL-C, and HDL-C), which were altered by ISO administration. Moreover, 7-hyd.HC precotreatment significantly mitigated the oxidative stress biomarkers, as evidenced by the decrease of lipid peroxidation and the increased level of the myocardial GSH level together with the SOD, GSH-Px, and catalase activities. 7-hyd.HC inhibited the cardiac apoptosis by upregulating the expression of Bcl-2 and downregulating the expression of Bax and caspase-3 genes. In addition, 7-hyd.HC reduced the elevated fibrinogen rate and better prevented the myocardial necrosis and improved the interstitial edema and neutrophil infiltration than sintrom. Overall, 7-hyd.HC ameliorated the severity of ISO-induced myocardial infarction through improving the oxidative status, attenuating apoptosis, and reducing fibrinogen production. The 7-hyd.HC actions could be mediated by its antioxidant, antiapoptotic, and anti-inflammatory capacities. The present study was directed to investigate the effect of precotreatment with (E)-N ′ -(1-(7-hydroxy-2-oxo-2H-chromen-3-yl) ethylidene) benzohydrazide (7-hyd.HC), a novel potent synthesized coumarin, on isoproterenol- (ISO-) induced myocardial infarction (MI) in rats. The hydrazone compound was characterized by IR, 1D, and 2D NMR analyses. Experimental induction of MI in rats was established by ISO (85 mg/kg/day, s.c) for two consecutive days (6th and 7th days). 7-hyd.HC or sintrom was given for 7 days prior and simultaneous to ISO injection. 7-hyd.HC offered a cardiopreventive effect by preventing heart injury marker leakage (LDH, ALT, AST, CK-MB, and cTn-I) from cardiomyocytes and normalizing cardiac function and ECG pattern, as well as improving lipid profile (TC, TG, LDL-C, and HDL-C), which were altered by ISO administration. Moreover, 7-hyd.HC precotreatment significantly mitigated the oxidative stress biomarkers, as evidenced by the decrease of lipid peroxidation and the increased level of the myocardial GSH level together with the SOD, GSH-Px, and catalase activities. 7-hyd.HC inhibited the cardiac apoptosis by upregulating the expression of Bcl-2 and downregulating the expression of Bax and caspase-3 genes. In addition, 7-hyd.HC reduced the elevated fibrinogen rate and better prevented the myocardial necrosis and improved the interstitial edema and neutrophil infiltration than sintrom. Overall, 7-hyd.HC ameliorated the severity of ISO-induced myocardial infarction through improving the oxidative status, attenuating apoptosis, and reducing fibrinogen production. The 7-hyd.HC actions could be mediated by its antioxidant, antiapoptotic, and anti-inflammatory capacities. |
| Author | Feryeni, Anwar Tir, Meriam Khdhiri, Emna Allouche, Noureddine Tlili, Nizar Ghazouani, Lakhdar Ammar, Houcine Abid, Souhir Hajji, Raouf Mnafgui, Kais Elmufti, Afoua |
| AuthorAffiliation | 6 Internal Medicine Department, Sidi Bouzid Hospital, Ibn Eljazzar Faculty of Medicine, University of Sousse, Sousse, Tunisia 4 Institut Supérieur des Sciences et Technologies de l'Environnement, Université de Carthage, Tunisia 8 Laboratory of Animal Physiology, Faculty of Sciences of Sfax, University of Sfax, P.O. Box 95, Sfax 3052, Tunisia 7 Laboratory of Organic Chemistry LR17ES08 (Natural Substances Team), Faculty of Sciences of Sfax, University of Sfax, Tunisia 1 Research Unit of Macromolecular Biochemistry and Genetics, Faculty of Sciences of Gafsa, 2112 Gafsa, Tunisia 3 Laboratoire d'Ecologie, de Biologie et de Physiologie des Organismes Aquatiques, LR18ES41, Faculté des Sciences de Tunis, Université Tunis EL Manar, 2092 Tunis, Tunisia 2 Laboratoire de Chimie Appliquée “Hétérocycles Corps Gras & Polymères”, Faculté des Sciences, Université de Sfax, 3038 Sfax, Tunisia 5 Département de Biologie (UR 13/ES25), Faculté des Sciences de Tunis, Université Tunis El-Manar, Tunis 2092, Tunisia |
| AuthorAffiliation_xml | – name: 6 Internal Medicine Department, Sidi Bouzid Hospital, Ibn Eljazzar Faculty of Medicine, University of Sousse, Sousse, Tunisia – name: 2 Laboratoire de Chimie Appliquée “Hétérocycles Corps Gras & Polymères”, Faculté des Sciences, Université de Sfax, 3038 Sfax, Tunisia – name: 8 Laboratory of Animal Physiology, Faculty of Sciences of Sfax, University of Sfax, P.O. Box 95, Sfax 3052, Tunisia – name: 3 Laboratoire d'Ecologie, de Biologie et de Physiologie des Organismes Aquatiques, LR18ES41, Faculté des Sciences de Tunis, Université Tunis EL Manar, 2092 Tunis, Tunisia – name: 7 Laboratory of Organic Chemistry LR17ES08 (Natural Substances Team), Faculty of Sciences of Sfax, University of Sfax, Tunisia – name: 1 Research Unit of Macromolecular Biochemistry and Genetics, Faculty of Sciences of Gafsa, 2112 Gafsa, Tunisia – name: 5 Département de Biologie (UR 13/ES25), Faculté des Sciences de Tunis, Université Tunis El-Manar, Tunis 2092, Tunisia – name: 4 Institut Supérieur des Sciences et Technologies de l'Environnement, Université de Carthage, Tunisia |
| Author_xml | – sequence: 1 fullname: Ghazouani, Lakhdar – sequence: 2 fullname: Mnafgui, Kais – sequence: 3 fullname: Abid, Souhir – sequence: 4 fullname: Ammar, Houcine – sequence: 5 fullname: Hajji, Raouf – sequence: 6 fullname: Tlili, Nizar – sequence: 7 fullname: Elmufti, Afoua – sequence: 8 fullname: Tir, Meriam – sequence: 9 fullname: Khdhiri, Emna – sequence: 10 fullname: Feryeni, Anwar – sequence: 11 fullname: Allouche, Noureddine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32215169$$D View this record in MEDLINE/PubMed |
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| Copyright | Copyright © 2020 Anouar Feriani et al. Copyright © 2020 Anouar Feriani et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0 Copyright © 2020 Anouar Feriani et al. 2020 |
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| Snippet | The present study was directed to investigate the effect of precotreatment with (E)-N′-(1-(7-hydroxy-2-oxo-2H-chromen-3-yl) ethylidene) benzohydrazide... The present study was directed to investigate the effect of precotreatment with (E)-N ′ -(1-(7-hydroxy-2-oxo-2H-chromen-3-yl) ethylidene) benzohydrazide... The present study was directed to investigate the effect of precotreatment with (E)-N'-(1-(7-hydroxy-2-oxo-2H-chromen-3-yl) ethylidene) benzohydrazide... |
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| SubjectTerms | Animals Anti-Inflammatory Agents - chemical synthesis Anti-Inflammatory Agents - chemistry Anti-Inflammatory Agents - therapeutic use Apoptosis Apoptosis - drug effects Benzopyrans - chemical synthesis Benzopyrans - chemistry Benzopyrans - therapeutic use Biomarkers - metabolism Coumarins - chemical synthesis Coumarins - chemistry Coumarins - therapeutic use Drug dosages Energy resources Ethanol Heart attacks Hydrazones - chemical synthesis Hydrazones - chemistry Hydrazones - therapeutic use Inflammation Inflammation - metabolism Isoproterenol - toxicity Male Molecular Structure Myocardial Infarction - chemically induced Myocardial Infarction - drug therapy Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardium - metabolism Oxidative stress Oxidative Stress - drug effects Rats Rats, Wistar Treatment Outcome |
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| Title | (E)-N′-(1-(7-Hydroxy-2-Oxo-2H-Chromen-3-Yl) Ethylidene) Benzohydrazide, a Novel Synthesized Coumarin, Ameliorates Isoproterenol-Induced Myocardial Infarction in Rats through Attenuating Oxidative Stress, Inflammation, and Apoptosis |
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