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September 27, 2019Frontiers in PharmacologyOpen Access

DiOHF blunts doxorubicin-induced cardiac dysfunction in mice, improving LVEF by ~18%.

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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

DCDanqi ChangHLHang LiQCQian Cheng

Discussion

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Member takes

Overview

Should not alter doxorubicin regimens; leaves open whether DiOHF cardioprotection translates to patients.

Structured PICO

Does 3',4'-dihydroxyflavonol (DiOHF) prevent doxorubicin-induced cardiotoxicity in H9C2 cells and BALB/c mice?

P
Population
120 female BALB/c mice (8-10 weeks old) subjected to doxorubicin-induced cardiotoxicity and followed for 7 days.
I
Intervention
3',4'-dihydroxyflavonol (DiOHF)
C
Comparator
Doxorubicin treatment without DiOHF
O
Outcome
Doxorubicin-induced cardiotoxicity (including ROS production, mitochondrial dysfunction, apoptosis, serum CK-MB level, myocardial fibrosis, and left ventricular function)surrogate

Main Result

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.

Limitations

  • Preclinical animal model; whether the insights gleaned apply to humans requires further investigation.

Cite This Study

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%.

synapsesocial.com/papers/6aa5ea615175d8ad943971eahttps://doi.org/10.3389/fphar.2019.01081
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Flavonoids from Hippophae rhamnoides Linn. Revert Doxorubicin-Induced Cardiotoxicity through Inhibition of Mitochondrial Dysfunction in H9c2 Cardiomyoblasts In Vitro2023 · 14 citations
  2. 2Protective effect of dioscin against doxorubicin-induced cardiotoxicity via adjusting microRNA-140-5p-mediated myocardial oxidative stress2018 · 202 citations
  3. 3Role of diosmin in preventing doxorubicin-induced cardiac oxidative stress, inflammation, and hypertrophy: A mechanistic approach2024 · 1 citations
  4. 4DHDK, a Plant-Derived Natural Small Molecule, Protects Against Doxorubicin-Induced Cardiotoxicity via the PPARG-CPT1B-FAO Axis2025 · 1 citations
  5. 5ANTI-CANCER DRUG DOXORUBICIN INDUCED CARDIOTOXICITY: UNDERSTANDING THE MECHANISMS INVOLVED IN ROS GENERATION RESULTING IN MITOCHONDRIAL DYSFUNCTION2020 · 7 citations