Research Article
Modulation of ECG, Myocardial Oxidative Stress Markers and Connexion 43 Expression by Ascorbic Acid and Ferulic Acid in Isoproterenol-Induced Myocardial Infarction in Rats
Emile F Metias1, Nisreen M Aboelmaaty1, Abdelaziz M Hussein1*, Eman W Abdallah1 and Azza Abdelaziz21Department of Physiology, Faculty of Medicine, Mansoura University, Egypt
2Department of Pathology, Faculty of Medicine, Mansoura University, Egypt
- Corresponding Author:
- Abdelaziz M Hussein
Department of Physiology
Faculty of Medicine
Mansoura University, Egypt
Tel: 201002421140
E-mail: zizomenna28@yahoo.com
Received date: November 09, 2016; Accepted date: November 11, 2016; Published date: December 19, 2016
Citation: Metias EF, Aboelmaaty NM, Hussein AM, Abdallah EW, Abdelaziz A (2016) Modulation of ECG, Myocardial Oxidative Stress Markers and Connexion 43 Expression by Ascorbic Acid and Ferulic Acid in Isoproterenol-Induced Myocardial Infarction in Rats. Biochem Physiol 5:210. doi:10.4172/2168-9652.1000210
Copyright: © 2016, Metias EF, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
Abstract
Objective: To assess the effects of ferulic acid (FeA) and ascorbic acid (AS) and combination of both on ECG variables, serum cardiac enzymes (AST, LDH, CK-MB), myocardial oxidative stress markers (MDA, SOD and GSH) and connexin 43 (Cx43) expressions in isoproterenol (ISO)-induced myocardial infarction. Methods: 40 male rats were equally allocated into 5 groups, 1) Control group, 2) ISO-induced MI group (rats received ISO 150 mg/Kg ip for 2 consecutive days at 24 h intervals), 3) FeA group (rats received ISO+FeA at 20 mg/kg/day po for 6 days), 4) AS group (rats received ISO+AS at 80 mg/kg/day po for 6 days) and 5) Combined group (rats received ISO+AS+FeA in the same previous doses). Results: The ISO group showed significant increase in serum cardiac enzymes (AST, CK-MB, and LDH), myocardial MDA and myocardial histopathological damage score with significant decrease in myocardial antioxidants (SOD and GSH) and Cx43expression compared to the control group (p<0.05). ECG traces of rats of ISO-induced MI, showed ST segment elevation, prolonged QT interval, shortened RR interval and increased heart rate. A combination of FeA and AS caused more significant improvement in the studied parameters than did each agent alone. ECG changes were improved significantly in the combined treatment group only. Conclusion: A combination of FeA and AS seems to offer a greater protective effect against ISO-induced myocardial infarction. This might be due to the synergism between their antioxidant properties as well as their effects on the density and location of Cx43 in myocardium.
