Taurine Ameliorates Iron Overload-Induced Hepatocyte Injury via the Bcl-2/VDAC1-Mediated Mitochondrial Apoptosis Pathway. (16th July 2022)

• Record Type: Journal Article
• Authors: Feng, Xiaoyu; Hu, Wenfeng; Hong, Yujiao; Ruan, Linlin; Hu, Yueben; Liu, Dan
• Other Names: Jia Zhihao Academic Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2022(2022)
• Publication Date: 2022-07-16
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2022/4135752
• Languages: English
• ISSNs: 1942-0900

Abstract

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.