Why the study?
Clinical use of doxorubicin is limited by cardiotoxicity, and the protective effects of the synthetic flavonoid DiOHF on doxorubicin-induced cardiotoxicity remained to be explored.
Does 3',4'-dihydroxyflavonol (DiOHF) prevent doxorubicin-induced cardiotoxicity in H9C2 cells and BALB/c mice?
Population
H9C2 cells and BALB/c mice
Comparison
DiOHF administration vs doxorubicin alone
Design
Preclinical in vitro and in vivo animal study
Key result
DiOHF administration blunted doxorubicin-induced cardiac dysfunction in mice, significantly improving left ventricular ejection fraction from 70.43% to 82.92%.
Authors
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Should not alter doxorubicin regimens; leaves open whether DiOHF cardioprotection translates to patients.
Does 3',4'-dihydroxyflavonol (DiOHF) prevent doxorubicin-induced cardiotoxicity in H9C2 cells and BALB/c mice?
Absolute Event Rate: 82.92% vs 70.43%
p-value: p=<0.05
DiOHF demonstrates protective effects against doxorubicin-induced cardiotoxicity in preclinical models by inhibiting ROS release, stabilizing mitochondrial function, and reducing apoptosis via ERK1 signaling activation.
Chang et al. (2019) studied Doxorubicin-induced cardiotoxicity (n=120). 3',4'-dihydroxyflavonol (DiOHF) vs. Doxorubicin alone was evaluated on Left ventricular ejection fraction (LVEF) at 7 days (p=<0.05). DiOHF administration blunted doxorubicin-induced cardiac dysfunction in mice, significantly improving left ventricular ejection fraction from 70.43% to 82.92%.
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