Cardiopreventive capacity of a novel (E)‐Nʹ‐(1‐(7‐methoxy‐2‐oxo‐2H‐chromen‐3‐yl) ethylidene)‐4‐methylbenzenesulfonohydrazide against isoproterenol‐induced myocardial infarction by moderating biochemical, oxidative stress, and histological parameters. Issue 6 (23rd February 2021)

• Record Type: Journal Article
• Authors: Khdhiri, Emna; Mnafgui, Kais; Ncir, Marwa; Feriani, Anouar; Ghazouani, Lakhdar; Hajji, Raouf; Jallouli, Dana; Abid, Majdi; Jamoussi, Kamel; Allouche, Noureddine; Ammar, Houcine; Abid, Souhir
• Is Part Of: Journal of biochemical and molecular toxicology. Volume 35:Issue 6(2021)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2021-02-23
• Subjects: coumarin -- myocardial infarction -- necrosis -- oxidative stress; Biochemistry -- Periodicals; Molecular biology -- Periodicals; Toxicology -- Periodicals; 574
• DOI: 10.1002/jbt.22747
• Languages: English
• ISSNs: 1095-6670

Abstract

Abstract: This study is carried out to assess the cardiopreventive effect of (E)‐N'‐(1‐(7‐methoxy‐2‐oxo‐2H‐chromen‐3‐yl) ethylidene)‐4‐methylbenzenesulfonohydrazide or SHC, a novel synthesized coumarin, against myocardial infarction induced by isoproterenol (ISO). The SHC compound was identified and characterized by spectral methods (infrared, 1 H NMR [nuclear magnetic resonance], 13 C NMR, Nuclear Overhauser Effect Spectroscopy, and high‐resolution mass spectroscopy). Male Wistar rats were divided into four groups: Control, ISO (rats were injected subcutaneously by 85 mg/kg body weight [BW] of isoproterenol at Days 6 and 7 of the experience), ISO + SHC (150 µg/kg BW, orally for 7 days) and ISO + acenocoumarol (150 µg/kg BW, orally for 7 days). Results showed that ISO induced a remarkable alteration of electrocardiogram (ECG) pattern and increases of plasma cardiac troponin T, creatine kinase‐MB, total cholesterol, triglycerides, low‐density lipoprotein‐cholesterol, lactate dehydrogenase, aspartate transaminase, and malondialdehyde. In addition, ISO reduced the high‐density lipoprotein‐cholesterol content and the activities of superoxide dismutase and glutathione peroxidase, with the induction of myocardial necrosis. However, SHC administration revealed a significant decrease in cardiac dysfunction markers, restored normal ECG pattern, as well as improving lipids parameters. Moreover, SHC treatment remarkably alleviated the cardiac oxidative stress and the myocardial remodeling process. Overall, the SHC offers good protection from acute myocardial infarction through the antioxidant capacity.