Introduction: Myocardial infarction (MI) remains one of the most common and life-threatening cardiovascular diseases worldwide. Experimental models of MI are essential for understanding its pathophysiology and evaluating therapeutic interventions. Objective: The aim of this study was to evaluate lipid peroxidation and antioxidant defense during experimental MI in rats. Methods: MI was induced in adult male rats by ligation of the left coronary artery. On the third day after MI, cardiac and liver tissues were collected. Heart and liver homogenates, as well as mitochondrial (MF) and microsomal (MSF) fractions of the liver, were analyzed for malondialdehyde (MDA) concentration and superoxide dismutase (SOD) activity. Results: Compared with the control group, MDA concentration increased fivefold in cardiac homogenates and 6.1-fold in liver MF, while MSF showed the most pronounced increase (28.2-fold). SOD activity was significantly reduced: by 31.5% in MF and by 73.1% in MF. Conclusion: Experimental MI induces pronounced oxidative stress, characterized by excessive lipid peroxidation and suppression of antioxidant defenses. This model represents a valuable tool for investigating cardioprotective strategies and antioxidant therapy.
| Published in | International Journal of Cardiovascular and Thoracic Surgery (Volume 12, Issue 1) |
| DOI | 10.11648/j.ijcts.20261201.13 |
| Page(s) | 14-17 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2026. Published by Science Publishing Group |
Myocardial Infarction, Oxidative Stress, Lipid Peroxidation, Malondialdehyde, Superoxide Dismutase, Experimental Model
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APA Style
Kenjayevich, B. A. (2026). Oxidative Stress and Lipid Peroxidation in Experimental Myocardial Infarction: Biochemical Evaluation in Cardiac and Hepatic Tissue. International Journal of Cardiovascular and Thoracic Surgery, 12(1), 14-17. https://doi.org/10.11648/j.ijcts.20261201.13
ACS Style
Kenjayevich, B. A. Oxidative Stress and Lipid Peroxidation in Experimental Myocardial Infarction: Biochemical Evaluation in Cardiac and Hepatic Tissue. Int. J. Cardiovasc. Thorac. Surg. 2026, 12(1), 14-17. doi: 10.11648/j.ijcts.20261201.13
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Download@article{10.11648/j.ijcts.20261201.13,
author = {Baykulov Azim Kenjayevich},
title = {Oxidative Stress and Lipid Peroxidation in Experimental Myocardial Infarction: Biochemical Evaluation in Cardiac and Hepatic Tissue},
journal = {International Journal of Cardiovascular and Thoracic Surgery},
volume = {12},
number = {1},
pages = {14-17},
doi = {10.11648/j.ijcts.20261201.13},
url = {https://doi.org/10.11648/j.ijcts.20261201.13},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijcts.20261201.13},
abstract = {Introduction: Myocardial infarction (MI) remains one of the most common and life-threatening cardiovascular diseases worldwide. Experimental models of MI are essential for understanding its pathophysiology and evaluating therapeutic interventions. Objective: The aim of this study was to evaluate lipid peroxidation and antioxidant defense during experimental MI in rats. Methods: MI was induced in adult male rats by ligation of the left coronary artery. On the third day after MI, cardiac and liver tissues were collected. Heart and liver homogenates, as well as mitochondrial (MF) and microsomal (MSF) fractions of the liver, were analyzed for malondialdehyde (MDA) concentration and superoxide dismutase (SOD) activity. Results: Compared with the control group, MDA concentration increased fivefold in cardiac homogenates and 6.1-fold in liver MF, while MSF showed the most pronounced increase (28.2-fold). SOD activity was significantly reduced: by 31.5% in MF and by 73.1% in MF. Conclusion: Experimental MI induces pronounced oxidative stress, characterized by excessive lipid peroxidation and suppression of antioxidant defenses. This model represents a valuable tool for investigating cardioprotective strategies and antioxidant therapy.},
year = {2026}
}
TY - JOUR T1 - Oxidative Stress and Lipid Peroxidation in Experimental Myocardial Infarction: Biochemical Evaluation in Cardiac and Hepatic Tissue AU - Baykulov Azim Kenjayevich Y1 - 2026/02/02 PY - 2026 N1 - https://doi.org/10.11648/j.ijcts.20261201.13 DO - 10.11648/j.ijcts.20261201.13 T2 - International Journal of Cardiovascular and Thoracic Surgery JF - International Journal of Cardiovascular and Thoracic Surgery JO - International Journal of Cardiovascular and Thoracic Surgery SP - 14 EP - 17 PB - Science Publishing Group SN - 2575-4882 UR - https://doi.org/10.11648/j.ijcts.20261201.13 AB - Introduction: Myocardial infarction (MI) remains one of the most common and life-threatening cardiovascular diseases worldwide. Experimental models of MI are essential for understanding its pathophysiology and evaluating therapeutic interventions. Objective: The aim of this study was to evaluate lipid peroxidation and antioxidant defense during experimental MI in rats. Methods: MI was induced in adult male rats by ligation of the left coronary artery. On the third day after MI, cardiac and liver tissues were collected. Heart and liver homogenates, as well as mitochondrial (MF) and microsomal (MSF) fractions of the liver, were analyzed for malondialdehyde (MDA) concentration and superoxide dismutase (SOD) activity. Results: Compared with the control group, MDA concentration increased fivefold in cardiac homogenates and 6.1-fold in liver MF, while MSF showed the most pronounced increase (28.2-fold). SOD activity was significantly reduced: by 31.5% in MF and by 73.1% in MF. Conclusion: Experimental MI induces pronounced oxidative stress, characterized by excessive lipid peroxidation and suppression of antioxidant defenses. This model represents a valuable tool for investigating cardioprotective strategies and antioxidant therapy. VL - 12 IS - 1 ER -
Department of Pharmaceutical and Toxicological Chemistry, Samarkand State Medical University, Uzbekistan, Samarkand
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