Natural compounds against doxorubicin-induced cardiotoxicity: A review on the involvement of Nrf2/ARE signaling pathway.
Fatemeh YarmohammadiRamin RezaeeGholamreza KarimiPublished in: Phytotherapy research : PTR (2020)
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.
Keyphrases
- oxidative stress
- diabetic rats
- signaling pathway
- reactive oxygen species
- high glucose
- nuclear factor
- induced apoptosis
- dna damage
- ischemia reperfusion injury
- drug delivery
- epithelial mesenchymal transition
- toll like receptor
- drug induced
- cell death
- pi k akt
- endothelial cells
- atrial fibrillation
- heat stress
- endoplasmic reticulum stress
- water soluble