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Objective <p>Cardiovascular diseases are significant health problems that cause high mortality rates worldwide. Myocardial infarction (MI), in particular, is one of the leading conditions among these diseases. The aim of this study is to evaluate the potential therapeutic approach of carvacrol in the treatment of cardiovascular diseases by investigating its protective effects against myocardial infarction through oxidative stress and biomarker levels.</p> Materials and methods <p>In this study, 28 male Wistar albino rats were used, and divided into 4 groups: Control, Carvacrol, Myocardial Infarction (MI), and MI + Carvacrol. Carvacrol was administered at a dose of 50&#xa0;mg/kg for six weeks. The induction of MI was performed during the last 2 days of carvacrol administration by administering 100&#xa0;mg/kg isoproterenol subcutaneously. At the end of the experiment, blood pressure, biomarkers such as troponin T, BNP, GDF-15, and IL-6 were measured, and cardiac tissue was histopathologically examined.</p> Results <p>The results show that in the MI group, troponin T, BNP, IL-6 and GDF-15 levels were increased, while diastolic blood pressure and heart rate were decreased. In the carvacrol-treated group, troponin T, BNP, IL-6 and GDF-15 levels were decreased. Carvacrol did not significantly affect systolic, diastolic, mean arterial pressure, or heart rate in experimental groups. Moreover, carvacrol decreased necrosis, edema, and mononuclear cell infiltration in the heart tissue, which were increased due to MI.</p> Conclusion <p>In conclusion, carvacrol demonstrated protective effects against myocardial infarction. Carvacrol alleviated histopathological damage by reducing inflammatory biomarkers. In addition to carvacrol improved troponin T and BNP markers.These findings suggest that carvacrol may be a promising agent in the treatment of cardiovascular diseases. However, more comprehensive and long-term studies are needed to confirm this effect and transfer it to clinical applications. </p>

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Cardioprotective effects of carvacrol in the isoproterenol-induced myocardial infarction model

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月14日

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  • Seda Koçak,
  • Kübra Tuğçe Kalkan,
  • Ömürcan Sadettin Aydın,
  • Kübra Öztürk

摘要

Objective

Cardiovascular diseases are significant health problems that cause high mortality rates worldwide. Myocardial infarction (MI), in particular, is one of the leading conditions among these diseases. The aim of this study is to evaluate the potential therapeutic approach of carvacrol in the treatment of cardiovascular diseases by investigating its protective effects against myocardial infarction through oxidative stress and biomarker levels.

Materials and methods

In this study, 28 male Wistar albino rats were used, and divided into 4 groups: Control, Carvacrol, Myocardial Infarction (MI), and MI + Carvacrol. Carvacrol was administered at a dose of 50 mg/kg for six weeks. The induction of MI was performed during the last 2 days of carvacrol administration by administering 100 mg/kg isoproterenol subcutaneously. At the end of the experiment, blood pressure, biomarkers such as troponin T, BNP, GDF-15, and IL-6 were measured, and cardiac tissue was histopathologically examined.

Results

The results show that in the MI group, troponin T, BNP, IL-6 and GDF-15 levels were increased, while diastolic blood pressure and heart rate were decreased. In the carvacrol-treated group, troponin T, BNP, IL-6 and GDF-15 levels were decreased. Carvacrol did not significantly affect systolic, diastolic, mean arterial pressure, or heart rate in experimental groups. Moreover, carvacrol decreased necrosis, edema, and mononuclear cell infiltration in the heart tissue, which were increased due to MI.

Conclusion

In conclusion, carvacrol demonstrated protective effects against myocardial infarction. Carvacrol alleviated histopathological damage by reducing inflammatory biomarkers. In addition to carvacrol improved troponin T and BNP markers.These findings suggest that carvacrol may be a promising agent in the treatment of cardiovascular diseases. However, more comprehensive and long-term studies are needed to confirm this effect and transfer it to clinical applications.