Eugenol attenuates paclitaxel-induced cardiotoxicity by modulating autophagy-related markers in rats.

Q: What are the key findings of this study?

Eugenol administration (25 mg/kg/day) following paclitaxel exposure significantly reduced serum brain natriuretic peptide levels by 53.67% and attenuated histopathological indicators of myocardial injury.

Q: What is the clinical evidence from this study?

Population: Paclitaxel-induced cardiotoxicity (n=36). Intervention: Eugenol vs. Paclitaxel alone and Vehicle (Saline). Primary outcome: Serum Brain Natriuretic Peptide (BNP) levels (p=<0.001).

Q: What does this research mean for the field?

Eugenol administration attenuates paclitaxel-induced cardiotoxicity in rats by improving hemodynamics, decreasing cardiac injury biomarkers, and normalizing autophagy-related protein expression. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To investigate the protective efficacy of eugenol against paclitaxel-induced myocardial damage and evaluate its effects on autophagy-related signaling pathways.

Halime Tozak Yıldız; Sadik Kucukgunay; Oya Korkmaz; Seda Koçak; Mustafa Numan Bucak

doi:10.22038/ijbms.2026.89478.19317

January 1, 2026Open Access

Eugenol attenuates paclitaxel-induced cardiotoxicity by modulating autophagy-related markers in rats.

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Key result

Eugenol reduces serum BNP by ~54% and attenuates paclitaxel-induced myocardial injury in preclinical models.

P<0.001
n=36

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Why the study?

Paclitaxel causes cardiotoxicity characterized by oxidative stress, inflammation, mitochondrial dysfunction, and disrupted autophagy and apoptosis, prompting investigation into the therapeutic potential of eugenol against this damage.

Does eugenol reduce paclitaxel-induced cardiotoxicity in a rat model?

Key Points

To investigate the protective efficacy of eugenol against paclitaxel-induced myocardial damage and evaluate its effects on autophagy-related signaling pathways.
Assessed hemodynamic parameters (systolic and diastolic blood pressure, mean arterial pressure, heart rate) and measured serum cardiac injury biomarkers (cTnT and BNP).
Conducted histopathological assessments via hematoxylin and eosin and iron hematoxylin staining alongside immunohistochemical analysis of mTOR, ULK1, and Atg13 expression.
Paclitaxel reduced mean arterial pressure compared to controls (P<0.001), while PTX+EUG5 and PTX+EUG25 increased MAP by 18.9% and 19.3%, respectively (both P<0.05).
Eugenol significantly reduced cardiac biomarkers versus PTX alone, decreasing cTnT by 10.02% (P=0.021) and 17.18% (P<0.001), and BNP by 32.99% and 53.67% (both P<0.001) in the EUG5 and EUG25 co-treatment groups.
Paclitaxel decreased mTOR expression (P<0.01) and elevated ULK1 and Atg13 (P<0.001), whereas EUG co-treatment significantly increased mTOR (P<0.001) and reduced ULK1 (P<0.05 for EUG5, P<0.001 for EUG25) and Atg13 (P<0.001).

Structured PICO

Does eugenol reduce paclitaxel-induced cardiotoxicity in a rat model?

P

Population

Thirty-six male Wistar rats (8-10 weeks old) were assigned to various paclitaxel and eugenol treatment groups over a 15-day period to investigate eugenol's protective effects against chemotherapy-induced cardiotoxicity.

I

Intervention

Eugenol at a dose of 5 mg/kg/day or 25 mg/kg/day via oral gavage for 10 consecutive days (days 6-15) following paclitaxel exposure

C

Comparator

Paclitaxel group (received paclitaxel 2 mg/kg/day IP for days 1-5 with no subsequent eugenol treatment) and Control group (received physiological saline vehicle)

O

Outcome

Hemodynamic parameters (systolic and diastolic blood pressure, heart rate, mean arterial pressure), serum cardiac biomarkers (cTnT and BNP), histopathological alterations, and immunohistochemical expression of autophagy-related proteins (mTOR, ULK1, and Atg13) at day 16surrogate

Main Result

p-value: p=<0.001

Eugenol attenuates paclitaxel-induced myocardial structural damage and biomarker elevation in a rat model, partly by modulating autophagy-related pathways.

Limitations

No functional cardiac assessments (such as echocardiography) were performed to confirm functional recovery.
The overall findings do not indicate a consistent dose-dependent response across all evaluated outcomes.
Modest cardiovascular/hemodynamic improvement suggests only partial modulation of intracellular dysregulation.
No functional cardiac assessments were performed
Short-term eugenol administration

Implication

Eugenol may attenuate paclitaxel cardiotoxicity in rats; hypothesis-generating and should not yet change clinical practice.

Abstract

Objectives: Paclitaxel (PTX) is a commonly used chemotherapeutic agent that causes cardiotoxicity characterized by oxidative stress, inflammation, and mitochondrial dysfunction, which disrupts autophagy and apoptosis in cardiomyocytes. This study investigated the therapeutic potential of eugenol (EUG), a natural anti-oxidant and anti-inflammatory compound, against PTX-induced cardiac damage. Materials and Methods: Thirty-six male Wistar rats were randomly assigned to six groups: Control, EUG5, EUG25, PTX, PTX+EUG5, and PTX+EUG25. Hemodynamic parameters (systolic and diastolic blood pressure and heart rate), serum cardiac biomarkers (troponin T and brain natriuretic peptide), histopathological alterations, and immunohistochemical expression of autophagy-related proteins (mTOR, ULK1, and Atg13) were evaluated. Results: PTX administration significantly reduced arterial blood pressure and increased serum cardiac injury biomarkers, accompanied by marked myocardial structural damage. Histopathological analysis revealed myocardial degeneration, inflammation, edema, and tissue disorganization in the PTX group. In PTX-exposed rats treated with EUG, arterial blood pressure was higher, and serum cardiac injury biomarkers were lower than in the PTX group, accompanied by reduced histopathological scores. PTX exposure was associated with decreased mTOR expression and increased ULK1 and Atg13 immunoreactivity, while EUG-treated PTX groups showed values closer to those of the control group for these autophagy-related markers. Conclusion: EUG administration was associated with reduced biochemical and histopathological indicators of cardiac injury in PTX-exposed rats, along with changes in autophagy-related markers. These findings demonstrate that EUG treatment coincided with attenuation of PTX-induced cardiac injury at the biochemical and histopathological levels, suggesting its potential experimental value in models of chemotherapy-associated cardiotoxicity.

Discussion

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Cite This Study

Yıldız et al. (2026) studied Paclitaxel-induced cardiotoxicity (n=36). Eugenol vs. Paclitaxel alone and Vehicle (Saline) was evaluated on Serum Brain Natriuretic Peptide (BNP) levels (p=<0.001). Eugenol administration (25 mg/kg/day) following paclitaxel exposure significantly reduced serum brain natriuretic peptide levels by 53.67% and attenuated histopathological indicators of myocardial injury.

synapsesocial.com/papers/6a31570faf7cf7f8256b3d0a https://doi.org/10.22038/ijbms.2026.89478.19317

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Eugenol attenuates paclitaxel-induced cardiotoxicity by modulating autophagy-related markers in rats.

Figures

Key Points

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

Eugenol attenuates paclitaxel-induced cardiotoxicity by modulating autophagy-related markers in rats.

Figures

Key Points

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

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