Why the study?
Cardiotoxicity from ROS generation and oxidative stress is the main concern for long-term doxorubicin use, and Nrf2 acts as a protective player against this myocardial oxidative damage.
Do natural compounds protect against doxorubicin-induced cardiotoxicity through the Nrf2 signaling pathway?
Do natural compounds protect against doxorubicin-induced cardiotoxicity through the Nrf2 signaling pathway?
Natural compounds may offer a protective strategy against doxorubicin-induced cardiotoxicity by targeting the Nrf2 oxidative stress pathway.
Natural compounds may support Nrf2-targeted cardioprotection in doxorubicin therapy; leaves open clinical translation pending trials.
Cardiotoxicity is the main concern for long-term use of the doxorubicin (DOX). Reactive oxygen species (ROS) generation leads to oxidative stress that significantly contributes to the cardiac damage induced by DOX. The nuclear factor erythroid 2-related factor (Nrf2) acts as a protective player against DOX-induced myocardial oxidative stress. Several natural compounds (NCs) with anti-oxidative effects, were examined to suppress DOX cardiotoxicity such as asiatic acid, α-linolenic acid, apigenin, baicalein, β-lapachone, curdione, dioscin, ferulic acid, Ganoderma lucidum polysaccharides, genistein, ginsenoside Rg3, indole-3-carbinol, naringenin-7-O-glucoside, neferine, p-coumaric acid, pristimerin, punicalagin, quercetin, sulforaphane, and tanshinone IIA. The present article, reviews NCs that showed protective effects against DOX-induced cardiac injury through induction of Nrf2 signaling pathway.
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Yarmohammadi et al. (2020) studied this question.
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