Key result
Artemisia dracunculus extract attenuates doxorubicin-induced cardiotoxicity across functional, oxidative, and inflammatory markers.
Why the study?
Doxorubicin-induced cardiotoxicity limits its clinical use, and protective effects of Artemisia dracunculus L. extract against this toxicity need investigation.
Does Artemisia dracunculus L. extract protect against doxorubicin-induced cardiotoxicity in a rat model?
Does Artemisia dracunculus L. extract protect against doxorubicin-induced cardiotoxicity in a rat model?
p-value: p=q < 0.05 to q < 0.001
Artemisia dracunculus L. extract demonstrates cardioprotective effects against doxorubicin-induced toxicity in rats by mitigating oxidative stress, inflammation, and fibrosis.
Doxorubicin (DOX), an extensively used anthracycline anticancer drug, can lead to toxicity in various body organs, especially the heart, which limits its clinical use. We aimed to investigate the protective effects of Artemisia dracunculus L. extract (ADE) against DOX-induced cardiotoxicity. This investigation was conducted on 48 male Wistar rats divided into six groups: Sham, Vehicle (DOX intraperitoneally 2 mg/kg every 48 h for 12 days), ADE groups (DOX + ADE orally 50, 100 and 200 mg/kg/day), positive control (DOX + Vitamin E orally 100 mg/kg/day) for 20 days and starting from four days before DOX. Transthoracic echocardiography, heart damage biomarkers, histological evaluations, oxidative stress, inflammatory, anti-inflammatory, and fibrotic markers were assessed. Our results revealed that DOX remarkably decreased body weight, heart tissue weight, glutathione (GSH), and interleukin (IL)-10 levels while increasing lactate dehydrogenase (LDH), troponin, creatine kinase (CK-MB), malondialdehyde (MDA), IL-6, TNF-α, TGF-β, and histopathological damage in heart tissue (q < 0.001 for all). Additionally, DOX significantly increased left ventricular (LV) end-systolic diameter (LVESd) and LV end-diastolic diameter (LVEDD) while decreasing LV fractional shortening (LVFS) and LV ejection fraction (LVEF) rather than the sham group (q < 0.001 for all). Nonetheless, treatment consisting of all three doses of ADE and vitamin E meaningfully ameliorated all these changes following the DOX-induced cardiotoxicity (q < 0.05 to q < 0.001). ADE effectively ameliorated DOX-induced cardiotoxicity through anti-oxidative, anti-inflammatory, and anti-fibrotic properties. Therefore, ADE may be considered a suitable candidate for treating many heart diseases. Howbeit, more clinical investigations are needed to verify its effectiveness.
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Toumari et al. (2026) studied Doxorubicin-induced cardiotoxicity (n=48). Artemisia dracunculus L. extract (ADE) vs. Vehicle (Doxorubicin alone) was evaluated on Echocardiographic parameters, heart damage biomarkers, histological evaluations, and oxidative/inflammatory markers (p=q < 0.05 to q < 0.001). Artemisia dracunculus L. extract significantly ameliorated doxorubicin-induced cardiotoxicity, improving echocardiographic, oxidative stress, inflammatory, and fibrotic markers (q < 0.05 to q < 0.001).
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