What does this research mean for the field?

Menthol treatment significantly reduces doxorubicin-induced cardiac injury by suppressing oxidative stress and inflammation in rats. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.SUPPORTS_CONSENSUS.

What question did this study set out to answer?

The study aims to evaluate menthol as a protective agent against doxorubicin-induced cardiotoxicity.

January 10, 2026Pharmaceuticals0 citationsOpen Access

Protective Role of Menthol Against Doxorubicin-Induced Cardiac Injury Through Suppression of TLR4/MAPK/NF-κB Signaling and Oxidative Stress

MMMark MansourAl-Azhar University AAAhmed AshourManchester Academic Health Science Centre AGAmany M. GadSinai University

Key Result

Menthol treatment significantly suppressed oxidative stress and inflammation, reducing doxorubicin-induced cardiac injury in rats (p < 0.05).

Key Points

The study aims to evaluate menthol as a protective agent against doxorubicin-induced cardiotoxicity.
Allocated 40 rats into four groups: normal control, DOX-treated, DOX + menthol, menthol-only.
Administered DOX at 15 mg/kg intraperitoneally and menthol at 100 mg/kg orally for 7 days.
Collected cardiac tissues and sera for biochemical assays, histopathology, and immunohistochemistry.
Assessed oxidative stress markers (MDA, GSH) and inflammatory pathways (TLR4, MAPK, NF-κB).
Doxorubicin treatment increased serum troponin levels and oxidative stress markers significantly.
Menthol treatment notably reduced oxidative stress markers and inflammatory pathway activity.
Apoptosis indicators (P53 and caspase-3) were also significantly lowered with menthol treatment.

Structured PICO

Does menthol reduce doxorubicin-induced cardiac injury in a rat model?

Population

40 rats in a model of doxorubicin-induced cardiotoxicity

Intervention

Menthol 100 mg/kg orally for 7 days following doxorubicin injection

Comparator

Doxorubicin alone (15 mg/kg intraperitoneally), normal control, and menthol-only

Outcome

Biochemical assays (serum troponin), histopathological analysis, and immunohistochemistry for oxidative stress, inflammatory pathways, and apoptotic markerssurrogate

Menthol may serve as a promising adjunctive therapy to reduce doxorubicin-induced cardiotoxicity by suppressing TLR4/MAPK/NF-κB signaling and oxidative stress.

Main Result

Absolute Event Rate: 0% vs 0%

Abstract

Background/Objectives: Doxorubicin (DOX) is a highly effective chemotherapeutic agent whose clinical use is limited by dose-dependent cardiotoxicity. This study aimed to investigate the potential protective effects of menthol against doxorubicin-induced cardiotoxicity (DIC) in a rat model. Methods: Forty rats were arbitrarily allocated into four groups: (1) normal control, (2) DOX-treated, (3) DOX + menthol treatment, and (4) menthol-only treatment. DOX (15 mg/kg) was applied intraperitoneally, and menthol (100 mg/kg) was applied orally for 7 days following the DOX injection. Cardiac tissue specimens and sera were collected for biochemical assays, histopathological analysis, and immunohistochemistry. Biomarkers of oxidative stress (MDA, GSH), inflammatory pathways (TLR4, MAPK, NF-κB, SREBP-1C), and apoptotic markers (P53, caspase-3) were assessed. Results: DOX employment caused remarkable rise in serum troponin levels (6.53 ± 0.98, p < 0.05), oxidative stress markers, and inflammatory proteins, alongside histopathological damage in cardiac tissues. Menthol treatment significantly suppressed oxidative stress (MDA, GSH), inflammation (TLR4, MAPK, NF-κB, SREBP-1C levels), and attenuated apoptosis (P53 and caspase-3 expression) (p < 0.05). Conclusions: Menthol may serve as a promising adjunctive therapy to reduce DOX cardiotoxicity without compromising DOX’s anticancer efficacy.

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