The Protective Role of Resveratrol against Arsenic Trioxide-Induced Cardiotoxicity
Figure 6
Summary indicating involvement of oxidative stress responses and the possible mechanism associated with Nrf2-HO-1 in As2O3-induced injury. As2O3 induces the increase of ROS production from mitochondria in rat cardiac myocytes. ROS triggers Ca2+ accumulation, 8-OHdG formation, and GSH deficiency in cardiocytes. RSV scavenges ROS, reduces DNA damage (indicated with 8-OHdG), and preserves GSH and Ca2+ homeostasis. Additionally, Nrf2-HO-1, a key signaling pathway involved in cellular oxidative responses, is prohibited by RSV As2O3-induced downregulation. Taken together, RSV protects the integrity of cardiac myocytes after exposure to As2O3, thereby decreasing AST, CK, CK-MB, and LDH release, as well as facilitating arsenic efflux. Future studies are required to clarify the mechanism for protecting RSV against As2O3-induced cardiotoxicity in endoplasmic reticulum and mitochondria. ROS: reactive oxygen species; RSV: resveratrol; + or (+) stands for positive improvement or negative improvement.
