Key result
Pretreatment and co-treatment with p-coumaric acid partially restored the antioxidant system and mitigated Doxorubicin-induced cardiotoxicity without impeding its anti-tumor efficacy.
Why the study?
While p-coumaric acid (pCA) has shown cardioprotective potential against doxorubicin-mediated cardiotoxicity in normal animals, its effects on doxorubicin's cardiotoxic and anti-tumor activity in tumor-bearing models remained to be examined.
Does p-coumaric acid reduce doxorubicin-induced cardiotoxicity without interfering with anti-tumor activity in tumor-bearing and non-tumor-bearing mice?
Does p-coumaric acid reduce doxorubicin-induced cardiotoxicity without interfering with anti-tumor activity in tumor-bearing and non-tumor-bearing mice?
p-coumaric acid shows potential as a cardioprotective agent against doxorubicin-induced cardiotoxicity without compromising anti-tumor efficacy in a mouse model.
p-Coumaric acid may attenuate doxorubicin cardiotoxicity in mice without antitumor interference; leaves open clinical translation.
The cardioprotective potential of p-coumaric acid (pCA) against Doxorubicin (Dox)-mediated cardiotoxicity in normal animals has been previously documented. The present study sought to examine the effect of pCA on the cardiotoxic and anti-tumor activity of Dox in non-tumor vs. Daltons Lymphoma Ascites (DLA) induced solid tumor model. Male Swiss Albino mice were pretreated and co-treated with pCA (100 mg/kg b.w.), after which Dox (16 mg/kg b.w. cumulative) was administered for a period of 28 days. Levels of serum cardiac diagnostic markers, lipid peroxidation products, and liver marker enzymes were significantly increased (P<0.05) in the Dox only treated groups. Partial restoration of the antioxidant system in the pCA pre/co-treated groups was observed. Cardiac damage was elevated in the Dox only tumor group; evident from changes in the heart/body weight ratio, haematological and biochemical analyses. Dox treated groups showed a significant reduction in tumor progression. pCA treatment did not appear to impede/enhance the efficacy of Dox-mediated anti-tumor activity in the tumor supergroup. This study leads us to conclude that pCA can be explored as a potent molecule to combat Dox-induced cardiotoxicity by the virtue of its proven antioxidant properties with no interference in the anti-tumor activity of Dox at the given dose.
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Chacko et al. (2021) studied Doxorubicin-induced cardiotoxicity. p-Coumaric acid (pCA) vs. Doxorubicin only was evaluated on Levels of serum cardiac diagnostic markers, lipid peroxidation products, and liver marker enzymes (p=<0.05). Pretreatment and co-treatment with p-coumaric acid partially restored the antioxidant system and mitigated Doxorubicin-induced cardiotoxicity without impeding its anti-tumor efficacy.
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