Highly potent visnagin derivatives inhibit Cyp1 and prevent doxorubicin cardiotoxicity
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Population
Zebrafish model of doxorubicin cardiomyopathy, mouse model of acute doxorubicin-induced cardiotoxicity, and…
Comparison
Visnagin and its analogs, CYP1 inhibitors, AHR… vs Doxorubicin alone or saline/DMSO controls.
Design
Preclinical
Follow-up
40 hours (zebrafish), 24 hours (mice)
Authors
Discussion
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Implication
Potent CYP1-inhibiting visnagin analogs may mitigate doxorubicin cardiotoxicity; leaves open clinical translation and mechanism confirmation in humans.
Structured PICO
P
Population
Zebrafish model of doxorubicin cardiomyopathy, mouse model of acute doxorubicin-induced cardiotoxicity (n=45 mice), and cultured HL-1 cardiomyocytes.
I
Intervention
Visnagin and its analogs (specifically C23), CYP1 inhibitors, AHR inhibitors, and Cyp1a knockdown.
C
Comparator
Doxorubicin alone (with vehicle/carrier) or saline/DMSO controls.
O
Outcome
Rescue from doxorubicin cardiomyopathy phenotype (decreased cardiac contraction, pericardial edema, and decreased tail blood flow) in zebrafish, and reduction of cardiac apoptosis in mice.surrogate
Highly potent visnagin analogs protect against doxorubicin-induced cardiotoxicity in preclinical models by inhibiting the CYP1 pathway.
Cite This Study
Asnani et al. (2018) studied this question.
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