Key result
DIM attenuates doxorubicin-induced oxidative stress and apoptosis in mice via Nrf2 pathway activation.
Why the study?
Does 3,3'-diindolylmethane (DIM) prevent doxorubicin-induced cardiotoxicity and genotoxicity in mice?
Population
Mice with doxorubicin-induced toxicity
Comparison
3,3'-diindolylmethane 25 mg/kg b.w., p.o. vs Doxorubicin alone (5 mg/kg b.w., i.p.)
Design
Preclinical
Authors
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Hypothesis-generating for DIM cardioprotection in doxorubicin therapy; human trials needed before clinical consideration.
Does 3,3'-diindolylmethane (DIM) prevent doxorubicin-induced cardiotoxicity and genotoxicity in mice?
p-value: p=<.05
DIM demonstrates chemoprotective efficacy against doxorubicin-induced cardiotoxicity and genotoxicity in mice via activation of the Nrf2/ARE signaling pathway.
Hajra et al. (2017) studied Doxorubicin-induced toxicity. 3,3'-diindolylmethane (DIM) vs. Doxorubicin alone was evaluated on Nrf2-mediated activation of antioxidant response element (ARE) pathway (p=<.05). In mice, 3,3'-diindolylmethane (DIM) significantly attenuated doxorubicin-induced oxidative stress, DNA damage, and apoptosis, and stimulated Nrf2-mediated activation of the ARE pathway (p < .05).
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