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. 2025 Jul 1;26(1):295.
doi: 10.1186/s12882-025-04245-6.

The effect of carvacrol on kidney injury caused by isopreterenol-induced myocardial infarction

Affiliations

The effect of carvacrol on kidney injury caused by isopreterenol-induced myocardial infarction

Gülhan Ünlü et al. BMC Nephrol. .

Abstract

Background: Myocardial infarction is a major cause of morbidity and mortality, often leading to heart and kidney dysfunction. Despite advancements in treatment, the link between heart and kidney damage is poorly understood. This study aims to evaluate the potential protective effect of Carvacrol, a natural bioactive compound, on kidney injury induced by myocardial infarction.

Methods: In this experimental study, 32 male Wistar rats were divided into four groups: Control, Carvacrol (50 mg/kg), Myocardial Infarction (85 mg/kg isoproterenol), and Myocardial Infarction + Carvacrol (50 mg/kg Carvacrol + 85 mg/kg isoproterenol). Carvacrol was administered for six weeks, and myocardial infarction was induced with isoproterenol. Blood pressure, biochemical parametres (creatinin kinase, lactate dehydrogenase, urea, creatinine, GDF-15, IL-6), and kidney tissue histopathology were evaluated.

Results: Biochemical analysis showed increased Creatinin Kinase and Lactate Dehydrogenase levels in the Myocardial Infarction group compared to controls(p = 0.023, p = 0.020), with carvacrol reducing these markers. IL-6 and GDF-15 levels were elevated in both the Myocardial Infarction and Myocardial Infarction + Carvacrol groups (p = 0.009, p < 0.001). Blood pressure was significantly reduced in the Myocardial Infarction group. Histopathological examination revealed severe kidney damage in the Myocardial Infarction group, while Carvacrol treatment showed less kidney damage, with only mild tubular dilation and rare necrosis.

Conclusion: Carvacrol appears to have protective effects against kidney injury in myocardial infarction. It reduced myocardial injury markers and kidney damage, suggesting its potential therapeutic use in cardiorenal syndrome. Further studies are needed to understand its mechanisms and clinical applications in cardiovascular and renal diseases.

Keywords: Carvacrol; Isopreterenol; Kidneys; Myocardial infarction; Rat.

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Conflict of interest statement

Declarations. Ethics approval and consent to participate: The experiments were conducted in accordance with the revised Animals (Scientific Procedures) Act 1986 in the UK and Directive 2010/63/EU in Europe. Ethical approval was obtained from Kirsehir Ahi Evran University Local Ethics Committee for Animal Experiments (Aprroval number: 2024-08-7). Consest for publication: Not applicable. Competing interests: The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Body weight in experimental groups
Fig. 2
Fig. 2
Serum CK and LDH levels in Control, MI, MI + CRV and CRV. Data are presented as mean ± SEM (n = 8)
Fig. 3
Fig. 3
Serum Urea and Creatinine levels in Control, MI, MI + CRV and CRV. Data are presented as mean ± SEM (n = 8)
Fig. 4
Fig. 4
Renal tissue levels of IL-6 and GDF-15 in Control, MI, MI + CRV and CRV. Data are presented as mean ± SEM (n = 8)
Fig. 5
Fig. 5
Systolic blood pressure, diastolic blood pressure, mean arterial pressure, and heart rate values in Control, MI, MI + CRV and CRV. Data are presented as mean ± SEM (n = 8)
Fig. 6
Fig. 6
Kidney sections H&E staining, magnification: X20, Bar: 100 μm. Control group, kidney tissue, normal histological appearance. MI group, renal tissue, tubule epithelium and diffuse hydropic degeneration (arrowhead) and coagulation necrosis (red star), dilation in tubules (black star), degeneration in glomeruli (black arrow), hyperemia in veins (blue arrow) Mild level of hydropic degeneration in CRV + MI group tubule epithelium, CRV group, kidney tissue, normal histological appearance. Kidney sections PAS staining, magnification: X40, Bar: 100 μm. In the MI group, tubular basement membrane thickening and glycogen accumulation (blue arrow), bowman capsule basement membrane (black arrow) and glomerular basement membrane thickening and mesangial matrix increase (yellow arrow)

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References

    1. Moran AE, Forouzanfar MH, Roth GA, Mensah GA, Ezzati M, Murray CJ, et al. Temporal trends in ischemic heart disease mortality in 21 world regions, 1980 to 2010: the global burden of disease 2010 study. Circulation. 2014;129(14):1483–92. - PMC - PubMed
    1. Kurian GA, Rajagopal R, Vedantham S, Rajesh M. The role of oxidative stress in myocardial ischemia and reperfusion injury and remodeling: revisited. Oxidative Med Cell Longev. 2016;2016(1):1656450. - PMC - PubMed
    1. Costanzo MR. The cardiorenal syndrome in heart failure. Heart Fail Clin. 2020;16(1):81–97. - PubMed
    1. Ronco C, Di Lullo L. Cardiorenal syndrome. Heart Fail Clin. 2014;10(2):251–80. - PubMed
    1. Abdelzaher WY, Ahmed SM, Welson NN, Alsharif KF, Batiha GE-S, Labib DAA. Dapsone ameliorates isoproterenol-induced myocardial infarction via Nrf2/HO-1; TLR4/TNF-α signaling pathways and the suppression of oxidative stress, inflammation, and apoptosis in rats. Front Pharmacol. 2021;12:669679. - PMC - PubMed

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