article · Cells Tissues Organs
Doxorubicin is a common chemotherapy drug, but it causes significant damage to heart tissue. This study investigated whether an aqueous extract of cardamom could protect rat heart muscles against this toxicity. Thirty male rats were divided into three groups: a control group, a group receiving doxorubicin alone, and a group receiving cardamom extract alongside doxorubicin. Rats given only doxorubicin suffered severe myocardial damage, marked by cellular disruption, increased collagen deposition, heart function loss, elevated oxidative stress, inflammation, and cell death. Pre-treatment and concurrent administration of cardamom extract countered these harmful effects across all measured markers. Furthermore, cardamom promoted tissue regeneration and blood vessel growth by boosting vascular endothelial growth factor. The findings show that cardamom extract can alleviate doxorubicin-induced heart toxicity by curbing oxidative stress, inflammation, and apoptosis while encouraging angiogenesis.
Doxorubicin is widely prescribed for cancer treatment, yet its utility is often limited by severe heart damage. Identifying accessible protective agents is critical for safer oncology therapies. By demonstrating that a natural spice extract can mitigate cardiac injury and stimulate tissue repair mechanisms in animal models, this research highlights potential avenues to reduce harmful chemotherapy side effects.
This research is at an early experimental stage, tested solely in a small rat model. If validated through further pre-clinical and clinical testing, cardamom extract could serve as a supportive botanical therapeutic or dietary supplement formulated for cancer patients receiving doxorubicin. Pharmaceutical or nutraceutical developers targeting cardioprotective adjunct therapies would be the primary interested parties, though significant clinical testing remains necessary before any commercial application.
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This study was conducted to evaluate the potential cardioprotective effect of cardamom (CAR) against myocardial injuries induced by doxorubicin (DOX) in rats through investigation of histological alterations and the associated oxidative stress, apoptosis, inflammation, and angiogenesis. This study included 30 adult male albino rats that were randomized to 3 groups (n = 10/group): group I (control), group II (DOX) rats injected with DOX (2.5 mg/kg body weight [BW] i.p.) every other day for 2 weeks, and group III (CAR+DOX) received CAR extract (200 mg/kg BW) orally for 3 weeks, and 1 week later (starting from the 2nd week) they were injected with DOX (2.5 mg/kg BW i.p.) every other day for 2 weeks. Rats treated with DOX alone exhibited notable myocardial damage (discontinuity and disorganization of cardiac muscle fibers, mononuclear cell infiltration, and apparent increases in collagen fiber deposition) accompanied by loss of function (revealed by elevated serum levels of lactate dehydrogenase, creatine kinase, and cardiac troponin), induction of oxidative stress (indicated by higher levels of nitric oxide and malon-dialdehyde, and lower levels of superoxide dismutase, catalase, and glutathione peroxidase), apoptosis (evidenced by high caspase 3 activity and immunostaining), and inflammation (marked by high cardiac NFκB level). However, administration of CAR not only ameliorated all deleterious effects of DOX but also induced angiogenesis, as indicated by a significant increase in VEGF immunoreactivity. These data indicate that CAR could relieve DOX-induced cardiotoxicity, at least in part, via reductions in oxidative stress, apoptosis, and inflammation and increased tissue regeneration via induction of angiogenesis. Therefore, CAR could be a promising cytoprotective agent against DOX cardiotoxicity.
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DOI: 10.1159/000496109
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