[Retracted] Taurine Ameliorates Iron Overload‐Induced Hepatocyte Injury via the Bcl‐2/VDAC1‐Mediated Mitochondrial Apoptosis Pathway

Abstract

Iron overload can induce reactive oxygen species (ROS) burst and liver damage. Taurine can reduce ROS production and ameliorate liver injury caused by iron overload; however, the underlying molecular mechanism remains elusive. Herein, L02 cells treated with 120 μ M iron dextran for 48 h showed marked oxidative stress damage and significantly increased apoptosis. Taurine protected hepatocytes by stabilizing mitochondrial membranes and resisting oxidative stress damage caused by iron overload. However, transfection with siRNA Bcl‐2 virus abrogated the observed protective effects. Following treatment with taurine, B cell lymphoma‐2 (Bcl‐2) could inhibit the opening of the mitochondrial permeability transition pore (mPTP), subsequently stabilizing the mitochondrial membrane potential by interacting with voltage‐dependent anion channel 1 (VDAC1) of mPTP. The present study is the first to clarify the mechanism underlying taurine‐afforded hepatocyte protection against iron overload‐induced oxidative stress via Bcl‐2‐mediated inhibition of mPTP opening and the antiapoptotic pathway.