Document Type : Original Research Article

Authors

1 Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran

2 Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran

3 Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

4 Department of Immunology and Genetics, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran

5 Department of Basic Sciences and Health, Sarab Faculty of Medical Sciences, Sarab, East Azerbaijan, Iran

6 Department of Physiology, Faculty of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran

10.22038/ajp.2024.25089

Abstract

Objective: Animal studies have revealed that lipid accumulation in obese mice fed with a high-fat diet (HFD) leads to alterations in the structural and functional properties of cardiovascular tissues. The current study aimed to investigate apoptosis/anti-apoptotic markers in the heart tissue of rats fed with a HFD.
Materials and Methods: Twenty-four male Wistar rats (weighing approximately 180 grams) were randomly divided into three groups (n=8 each group), including the control group (C), the high-fat diet group (HFD), and the high-fat diet + carvacrol group (HFD + Carva). Animals received a standard or HFD to induce obesity for three months. From day 61 to 90 in the HFD+Carva group, carvacrol was injected intraperitoneally (50 mg/kg) every other day. At the end of the study, the heart tissue was examined for pathological changes and the mRNA levels of TNF-α, Bcl2, Bax, and caspase3 in the heart tissue by Real Time-PCR.
Results: HFD-induced obesity led to increased TNF-α, caspase-3, and Bax and decreased Bcl-2 expression levels in heart tissue. Furthermore, histopathological changes in intracytoplasmic vacuole accumulation were evident in the HFD-obese animals. Carvacrol treatment significantly decreased the expression of Bax, TNF-α, and caspase-3 and increased the expression of Bcl-2 in heart tissue.
Conclusion: In the findings, carvacrol was found to decrease the histopathological changes caused by HFD in heart tissue by suppressing the expression of genes involved in the apoptosis pathway.

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