A novel synthetised sulphonylhydrazone coumarin (E)‐4‐methyl‐N′‐(1‐(3‐oxo‐3H‐benzo[f]chromen‐2‐ yl)ethylidene)benzenesulphonohydrazide protect against isoproterenol‐induced myocardial infarction in rats by attenuating oxidative damage, biological changes and electrocardiogram
Coumarins and their derivatives are becoming a potential source for new drug discovery due to their vast array of biological activities. The present study was designed to investigate the cardioprotective effects of a newly synthesised coumarin, symbolised as 5,6‐PhSHC, against cardiac remodelling pr...
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| Published in: | Clinical and experimental pharmacology & physiology Vol. 49; no. 9; pp. 1010 - 1026 |
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| Main Authors: | , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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01.09.2022
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| ISSN: | 0305-1870, 1440-1681, 1440-1681 |
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| Abstract | Coumarins and their derivatives are becoming a potential source for new drug discovery due to their vast array of biological activities. The present study was designed to investigate the cardioprotective effects of a newly synthesised coumarin, symbolised as 5,6‐PhSHC, against cardiac remodelling process in isoproterenol (ISO) induced myocardial infarction (MI) in male Wistar rats by evaluating haematological, biochemical and cardiac biomarkers. Rats were pre/co‐treated with 5,6‐PhSHC or clopidogrel (150 μg/kg body weight) daily for a period of 7 days and then MI was induced by injecting ISO (85 mg/kg body weight), at an interval of 24 hours for 2 consecutive days, on the sixth and seventh days. The in vivo exploration indicated that the injection of 5,6‐PhSHC improved the electrocardiographic (ECG) pattern and prevented severe heart damage by reducing leakage of the cardiac injury markers, such as troponin‐T (cTn‐T), lactate dehydrogenase (LDH), and creatine kinase‐MB. The cellular architecture of cardiac sections, altered in the myocardium of infracted rats, was reversed by 5,6‐PhSHC treatment. Results showed that injection of 5,6‐PhSHC elicited significant cardioprotective effects by prevention of myocardium cell necrosis and inflammatory cells infiltration, along with marked decrease in plasma levels of fibrinogen. In addition, the total cholesterol, triglyceride, LDL‐c, and HDL profiles underwent remarkable beneficial changes. It was also interesting to note that 5,6‐PhSHC enhanced the antioxidative defence mechanisms by increasing myocardial glutathione (GSH) level, superoxide dismutase (SOD), and catalase (CAT) activities, together with reducing the levels of thiobarbituric‐acid‐reactive substances (TBARS), when compared with ISO‐induced rats. Taken together, these findings suggested a beneficial role for 5,6‐PhSHC against ISO‐induced MI in rats. Furthermore, in silico analysis showed that 5,6‐PhSHC possess high computational affinities (E‐value >−9.0 kcal/mol) against cyclooxygenase‐2 (PDB‐ID: 1CX2), vitamin K epoxide reductase (PDB‐ID: 3KP9), glycoprotein‐IIb/IIIa (PDB‐ID: 2VDM) and catalase (PDB‐ID: 1DGF). Therefore, the present study provided promising data that the newly synthesised coumarin can be useful in the design and synthesis of novel drug against myocardial infarction. |
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| AbstractList | Coumarins and their derivatives are becoming a potential source for new drug discovery due to their vast array of biological activities. The present study was designed to investigate the cardioprotective effects of a newly synthesised coumarin, symbolised as 5,6‐PhSHC, against cardiac remodelling process in isoproterenol (ISO) induced myocardial infarction (MI) in male
Wistar
rats by evaluating haematological, biochemical and cardiac biomarkers. Rats were pre/co‐treated with 5,6‐PhSHC or clopidogrel (150 μg/kg body weight) daily for a period of 7 days and then MI was induced by injecting ISO (85 mg/kg body weight), at an interval of 24 hours for 2 consecutive days, on the sixth and seventh days. The in vivo exploration indicated that the injection of 5,6‐PhSHC improved the electrocardiographic (ECG) pattern and prevented severe heart damage by reducing leakage of the cardiac injury markers, such as troponin‐T (cTn‐T), lactate dehydrogenase (LDH), and creatine kinase‐MB. The cellular architecture of cardiac sections, altered in the myocardium of infracted rats, was reversed by 5,6‐PhSHC treatment. Results showed that injection of 5,6‐PhSHC elicited significant cardioprotective effects by prevention of myocardium cell necrosis and inflammatory cells infiltration, along with marked decrease in plasma levels of fibrinogen. In addition, the total cholesterol, triglyceride, LDL‐c, and HDL profiles underwent remarkable beneficial changes. It was also interesting to note that 5,6‐PhSHC enhanced the antioxidative defence mechanisms by increasing myocardial glutathione (GSH) level, superoxide dismutase (SOD), and catalase (CAT) activities, together with reducing the levels of thiobarbituric‐acid‐reactive substances (TBARS), when compared with ISO‐induced rats. Taken together, these findings suggested a beneficial role for 5,6‐PhSHC against ISO‐induced MI in rats. Furthermore, in silico analysis showed that 5,6‐PhSHC possess high computational affinities (
E
‐value >−9.0 kcal/mol) against cyclooxygenase‐2 (PDB‐ID: 1CX2), vitamin K epoxide reductase (PDB‐ID: 3KP9), glycoprotein‐IIb/IIIa (PDB‐ID: 2VDM) and catalase (PDB‐ID: 1DGF). Therefore, the present study provided promising data that the newly synthesised coumarin can be useful in the design and synthesis of novel drug against myocardial infarction. Coumarins and their derivatives are becoming a potential source for new drug discovery due to their vast array of biological activities. The present study was designed to investigate the cardioprotective effects of a newly synthesised coumarin, symbolised as 5,6-PhSHC, against cardiac remodelling process in isoproterenol (ISO) induced myocardial infarction (MI) in male Wistar rats by evaluating haematological, biochemical and cardiac biomarkers. Rats were pre/co-treated with 5,6-PhSHC or clopidogrel (150 μg/kg body weight) daily for a period of 7 days and then MI was induced by injecting ISO (85 mg/kg body weight), at an interval of 24 hours for 2 consecutive days, on the sixth and seventh days. The in vivo exploration indicated that the injection of 5,6-PhSHC improved the electrocardiographic (ECG) pattern and prevented severe heart damage by reducing leakage of the cardiac injury markers, such as troponin-T (cTn-T), lactate dehydrogenase (LDH), and creatine kinase-MB. The cellular architecture of cardiac sections, altered in the myocardium of infracted rats, was reversed by 5,6-PhSHC treatment. Results showed that injection of 5,6-PhSHC elicited significant cardioprotective effects by prevention of myocardium cell necrosis and inflammatory cells infiltration, along with marked decrease in plasma levels of fibrinogen. In addition, the total cholesterol, triglyceride, LDL-c, and HDL profiles underwent remarkable beneficial changes. It was also interesting to note that 5,6-PhSHC enhanced the antioxidative defence mechanisms by increasing myocardial glutathione (GSH) level, superoxide dismutase (SOD), and catalase (CAT) activities, together with reducing the levels of thiobarbituric-acid-reactive substances (TBARS), when compared with ISO-induced rats. Taken together, these findings suggested a beneficial role for 5,6-PhSHC against ISO-induced MI in rats. Furthermore, in silico analysis showed that 5,6-PhSHC possess high computational affinities (E-value >-9.0 kcal/mol) against cyclooxygenase-2 (PDB-ID: 1CX2), vitamin K epoxide reductase (PDB-ID: 3KP9), glycoprotein-IIb/IIIa (PDB-ID: 2VDM) and catalase (PDB-ID: 1DGF). Therefore, the present study provided promising data that the newly synthesised coumarin can be useful in the design and synthesis of novel drug against myocardial infarction. Coumarins and their derivatives are becoming a potential source for new drug discovery due to their vast array of biological activities. The present study was designed to investigate the cardioprotective effects of a newly synthesised coumarin, symbolised as 5,6-PhSHC, against cardiac remodelling process in isoproterenol (ISO) induced myocardial infarction (MI) in male Wistar rats by evaluating haematological, biochemical and cardiac biomarkers. Rats were pre/co-treated with 5,6-PhSHC or clopidogrel (150 μg/kg body weight) daily for a period of 7 days and then MI was induced by injecting ISO (85 mg/kg body weight), at an interval of 24 hours for 2 consecutive days, on the sixth and seventh days. The in vivo exploration indicated that the injection of 5,6-PhSHC improved the electrocardiographic (ECG) pattern and prevented severe heart damage by reducing leakage of the cardiac injury markers, such as troponin-T (cTn-T), lactate dehydrogenase (LDH), and creatine kinase-MB. The cellular architecture of cardiac sections, altered in the myocardium of infracted rats, was reversed by 5,6-PhSHC treatment. Results showed that injection of 5,6-PhSHC elicited significant cardioprotective effects by prevention of myocardium cell necrosis and inflammatory cells infiltration, along with marked decrease in plasma levels of fibrinogen. In addition, the total cholesterol, triglyceride, LDL-c, and HDL profiles underwent remarkable beneficial changes. It was also interesting to note that 5,6-PhSHC enhanced the antioxidative defence mechanisms by increasing myocardial glutathione (GSH) level, superoxide dismutase (SOD), and catalase (CAT) activities, together with reducing the levels of thiobarbituric-acid-reactive substances (TBARS), when compared with ISO-induced rats. Taken together, these findings suggested a beneficial role for 5,6-PhSHC against ISO-induced MI in rats. Furthermore, in silico analysis showed that 5,6-PhSHC possess high computational affinities (E-value >-9.0 kcal/mol) against cyclooxygenase-2 (PDB-ID: 1CX2), vitamin K epoxide reductase (PDB-ID: 3KP9), glycoprotein-IIb/IIIa (PDB-ID: 2VDM) and catalase (PDB-ID: 1DGF). Therefore, the present study provided promising data that the newly synthesised coumarin can be useful in the design and synthesis of novel drug against myocardial infarction.Coumarins and their derivatives are becoming a potential source for new drug discovery due to their vast array of biological activities. The present study was designed to investigate the cardioprotective effects of a newly synthesised coumarin, symbolised as 5,6-PhSHC, against cardiac remodelling process in isoproterenol (ISO) induced myocardial infarction (MI) in male Wistar rats by evaluating haematological, biochemical and cardiac biomarkers. Rats were pre/co-treated with 5,6-PhSHC or clopidogrel (150 μg/kg body weight) daily for a period of 7 days and then MI was induced by injecting ISO (85 mg/kg body weight), at an interval of 24 hours for 2 consecutive days, on the sixth and seventh days. The in vivo exploration indicated that the injection of 5,6-PhSHC improved the electrocardiographic (ECG) pattern and prevented severe heart damage by reducing leakage of the cardiac injury markers, such as troponin-T (cTn-T), lactate dehydrogenase (LDH), and creatine kinase-MB. The cellular architecture of cardiac sections, altered in the myocardium of infracted rats, was reversed by 5,6-PhSHC treatment. Results showed that injection of 5,6-PhSHC elicited significant cardioprotective effects by prevention of myocardium cell necrosis and inflammatory cells infiltration, along with marked decrease in plasma levels of fibrinogen. In addition, the total cholesterol, triglyceride, LDL-c, and HDL profiles underwent remarkable beneficial changes. It was also interesting to note that 5,6-PhSHC enhanced the antioxidative defence mechanisms by increasing myocardial glutathione (GSH) level, superoxide dismutase (SOD), and catalase (CAT) activities, together with reducing the levels of thiobarbituric-acid-reactive substances (TBARS), when compared with ISO-induced rats. Taken together, these findings suggested a beneficial role for 5,6-PhSHC against ISO-induced MI in rats. Furthermore, in silico analysis showed that 5,6-PhSHC possess high computational affinities (E-value >-9.0 kcal/mol) against cyclooxygenase-2 (PDB-ID: 1CX2), vitamin K epoxide reductase (PDB-ID: 3KP9), glycoprotein-IIb/IIIa (PDB-ID: 2VDM) and catalase (PDB-ID: 1DGF). Therefore, the present study provided promising data that the newly synthesised coumarin can be useful in the design and synthesis of novel drug against myocardial infarction. Coumarins and their derivatives are becoming a potential source for new drug discovery due to their vast array of biological activities. The present study was designed to investigate the cardioprotective effects of a newly synthesised coumarin, symbolised as 5,6‐PhSHC, against cardiac remodelling process in isoproterenol (ISO) induced myocardial infarction (MI) in male Wistar rats by evaluating haematological, biochemical and cardiac biomarkers. Rats were pre/co‐treated with 5,6‐PhSHC or clopidogrel (150 μg/kg body weight) daily for a period of 7 days and then MI was induced by injecting ISO (85 mg/kg body weight), at an interval of 24 hours for 2 consecutive days, on the sixth and seventh days. The in vivo exploration indicated that the injection of 5,6‐PhSHC improved the electrocardiographic (ECG) pattern and prevented severe heart damage by reducing leakage of the cardiac injury markers, such as troponin‐T (cTn‐T), lactate dehydrogenase (LDH), and creatine kinase‐MB. The cellular architecture of cardiac sections, altered in the myocardium of infracted rats, was reversed by 5,6‐PhSHC treatment. Results showed that injection of 5,6‐PhSHC elicited significant cardioprotective effects by prevention of myocardium cell necrosis and inflammatory cells infiltration, along with marked decrease in plasma levels of fibrinogen. In addition, the total cholesterol, triglyceride, LDL‐c, and HDL profiles underwent remarkable beneficial changes. It was also interesting to note that 5,6‐PhSHC enhanced the antioxidative defence mechanisms by increasing myocardial glutathione (GSH) level, superoxide dismutase (SOD), and catalase (CAT) activities, together with reducing the levels of thiobarbituric‐acid‐reactive substances (TBARS), when compared with ISO‐induced rats. Taken together, these findings suggested a beneficial role for 5,6‐PhSHC against ISO‐induced MI in rats. Furthermore, in silico analysis showed that 5,6‐PhSHC possess high computational affinities (E‐value >−9.0 kcal/mol) against cyclooxygenase‐2 (PDB‐ID: 1CX2), vitamin K epoxide reductase (PDB‐ID: 3KP9), glycoprotein‐IIb/IIIa (PDB‐ID: 2VDM) and catalase (PDB‐ID: 1DGF). Therefore, the present study provided promising data that the newly synthesised coumarin can be useful in the design and synthesis of novel drug against myocardial infarction. Coumarins and their derivatives are becoming a potential source for new drug discovery due to their vast array of biological activities. The present study was designed to investigate the cardioprotective effects of a newly synthesised coumarin, symbolised as 5,6‐PhSHC, against cardiac remodelling process in isoproterenol (ISO) induced myocardial infarction (MI) in male Wistar rats by evaluating haematological, biochemical and cardiac biomarkers. Rats were pre/co‐treated with 5,6‐PhSHC or clopidogrel (150 μg/kg body weight) daily for a period of 7 days and then MI was induced by injecting ISO (85 mg/kg body weight), at an interval of 24 hours for 2 consecutive days, on the sixth and seventh days. The in vivo exploration indicated that the injection of 5,6‐PhSHC improved the electrocardiographic (ECG) pattern and prevented severe heart damage by reducing leakage of the cardiac injury markers, such as troponin‐T (cTn‐T), lactate dehydrogenase (LDH), and creatine kinase‐MB. The cellular architecture of cardiac sections, altered in the myocardium of infracted rats, was reversed by 5,6‐PhSHC treatment. Results showed that injection of 5,6‐PhSHC elicited significant cardioprotective effects by prevention of myocardium cell necrosis and inflammatory cells infiltration, along with marked decrease in plasma levels of fibrinogen. In addition, the total cholesterol, triglyceride, LDL‐c, and HDL profiles underwent remarkable beneficial changes. It was also interesting to note that 5,6‐PhSHC enhanced the antioxidative defence mechanisms by increasing myocardial glutathione (GSH) level, superoxide dismutase (SOD), and catalase (CAT) activities, together with reducing the levels of thiobarbituric‐acid‐reactive substances (TBARS), when compared with ISO‐induced rats. Taken together, these findings suggested a beneficial role for 5,6‐PhSHC against ISO‐induced MI in rats. Furthermore, in silico analysis showed that 5,6‐PhSHC possess high computational affinities (E‐value >−9.0 kcal/mol) against cyclooxygenase‐2 (PDB‐ID: 1CX2), vitamin K epoxide reductase (PDB‐ID: 3KP9), glycoprotein‐IIb/IIIa (PDB‐ID: 2VDM) and catalase (PDB‐ID: 1DGF). Therefore, the present study provided promising data that the newly synthesised coumarin can be useful in the design and synthesis of novel drug against myocardial infarction. |
| Author | Ramazani, Ali Abid, Majdi Allouche, Noureddine Tlili, Nizar Ammar, Houcine Mnafgui, Kais Khdhiri, Emna Ghazouani, Lakhdar Hajji, Raouf Abid, Souhir Feriani, Anouar Baaziz, Intissar Zarei, Armin Elmufti, Afoua |
| Author_xml | – sequence: 1 givenname: Lakhdar orcidid: 0000-0001-7457-9113 surname: Ghazouani fullname: Ghazouani, Lakhdar email: ghazouani2005@yahoo.fr organization: University of Gafsa – sequence: 2 givenname: Emna surname: Khdhiri fullname: Khdhiri, Emna organization: Université de Sfax – sequence: 3 givenname: Afoua surname: Elmufti fullname: Elmufti, Afoua organization: University of Gafsa – sequence: 4 givenname: Armin surname: Zarei fullname: Zarei, Armin organization: University of Zanjan – sequence: 5 givenname: Anouar surname: Feriani fullname: Feriani, Anouar organization: University of Gafsa – sequence: 6 givenname: Intissar surname: Baaziz fullname: Baaziz, Intissar organization: University of Gafsa – sequence: 7 givenname: Raouf surname: Hajji fullname: Hajji, Raouf organization: University of Sousse – sequence: 8 givenname: Majdi surname: Abid fullname: Abid, Majdi organization: Jouf University – sequence: 9 givenname: Houcine surname: Ammar fullname: Ammar, Houcine organization: Université de Sfax – sequence: 10 givenname: Souhir surname: Abid fullname: Abid, Souhir organization: Jouf University – sequence: 11 givenname: Noureddine surname: Allouche fullname: Allouche, Noureddine organization: University of Sfax – sequence: 12 givenname: Kais orcidid: 0000-0002-9551-6266 surname: Mnafgui fullname: Mnafgui, Kais organization: University of Sfax – sequence: 13 givenname: Ali surname: Ramazani fullname: Ramazani, Ali organization: University of Zanjan – sequence: 14 givenname: Nizar surname: Tlili fullname: Tlili, Nizar organization: University of Carthage |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35717592$$D View this record in MEDLINE/PubMed |
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| Keywords | cardioprotective activity molecular docking myocardial infarction isoproterenol coumarin derivative oxidative stress electrocardiography |
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| Snippet | Coumarins and their derivatives are becoming a potential source for new drug discovery due to their vast array of biological activities. The present study was... |
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| SubjectTerms | Animals Antioxidants - metabolism Biomarkers Body Weight Calcium-binding protein cardioprotective activity Cardiotonic Agents - adverse effects Catalase Catalase - metabolism Cholesterol Clopidogrel Computer applications Coumarin coumarin derivative Coumarins - pharmacology Coumarins - therapeutic use Creatine Creatine kinase Damage prevention Drug development EKG Electrocardiography Fibrinogen Glutathione Glutathione - metabolism Glycoproteins Heart Heart attacks Inflammation Injection Injury prevention Isoproterenol Isoproterenol - adverse effects Kinases L-Lactate dehydrogenase Lactate dehydrogenase Lactic acid Male molecular docking Myocardial infarction Myocardial Infarction - chemically induced Myocardial Infarction - drug therapy Myocardial Infarction - prevention & control Myocardium Myocardium - metabolism Necrosis Oxidative Stress Plasma levels Prostaglandin endoperoxide synthase Rats Rats, Wistar Reductases Superoxide dismutase Triglycerides Troponin |
| Title | A novel synthetised sulphonylhydrazone coumarin (E)‐4‐methyl‐N′‐(1‐(3‐oxo‐3H‐benzo[f]chromen‐2‐ yl)ethylidene)benzenesulphonohydrazide protect against isoproterenol‐induced myocardial infarction in rats by attenuating oxidative damage, biological changes and electrocardiogram |
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| Volume | 49 |
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