Key result
Plumbagin supplementation for 14 days attenuated doxorubicin-stimulated cardiotoxicity in rats by ameliorating cardiac damage markers, inflammatory markers, and apoptotic proteins.
Why the study?
The study was designed to investigate the therapeutic role of plumbagin, a bioactive compound with therapeutic benefits, against doxorubicin-stimulated cardiotoxicity.
Does plumbagin prevent myocardial damage in rats with doxorubicin-induced cardiotoxicity?
Does plumbagin prevent myocardial damage in rats with doxorubicin-induced cardiotoxicity?
Plumbagin demonstrates cardioprotective effects against doxorubicin-induced cardiotoxicity in a rat model by reducing inflammation and apoptosis.
Answers are grounded in this paper and cite their sources.
No immediate clinical use; leaves open translation of plumbagin's effects to human cardio-oncology trials.
Cardiovascular disease created enormous health and economic burdens worldwide, which is responsible for the highest mobility and mortality that results in nearly 6.2% of in-hospital deaths every year. Plumbagin is a major bioactive compound that occurs in the Plumbago indica and P. zeylanica with numerous therapeutic benefits. The current research exploration was planned to investigate the therapeutic role of plumbagin against doxorubicin stimulated cardiotoxicity in rats. The cardiotoxicity was stimulated to the rats by administering the 2.5 mg/kg of doxorubicin for 14 days with concurrent supplementation with plumbagin. The hemodynamic parameters were studied by using the tail-cuff plethysmography. The lipid peroxidation and antioxidant status was examined by the standard procedures. The myocardial function and damage markers were assessed with the help of commercial kits. The expression status of inflammatory markers and PI3K/Akt signaling markers were investigated by reverse transcription polymerase chain reaction (RT-PCR) and western blotting analysis, respectively. The plumbagin supplementation appreciably regained the body weight and heart weight of the investigational animals. Hemodynamic parameters and antioxidants statuses were escalated by the plumbagin treatment. The severe elevation in the cardiac damage markers and inflammatory markers were noticeably ameliorated by the plumbagin treatment. The plumbagin treatment also assuaged the overexpression of inflammatory and apoptotic proteins in the heart tissues of doxorubicin-challenged rats. The histopathological analysis revealed that the plumbagin appreciably protected the heart tissues from the doxorubicin-induced damages. The findings of this exploration evidenced that plumbagin treatment attenuated the doxorubicin-stimulated cardiotoxicity in rats.
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Li et al. (2020) studied Doxorubicin-induced cardiotoxicity. Plumbagin vs. Doxorubicin alone was evaluated on Cardiotoxicity (hemodynamic parameters, antioxidant status, cardiac damage markers, inflammatory and apoptotic proteins). Plumbagin supplementation for 14 days attenuated doxorubicin-stimulated cardiotoxicity in rats by ameliorating cardiac damage markers, inflammatory markers, and apoptotic proteins.
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