ReferenceID 6295

Taurine Ameliorates Iron Overload-Induced Hepatocyte Injury via the Bcl-2/VDAC1-Mediated Mitochondrial Apoptosis Pathway

Oxid Med Cell Longev

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 el

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Reference Id
6295
Evidence Id
22885
Core Evidence Id
22885
Source Reference Id
5868
Herb2 Reference Id
HBREF006665
Subject Paper Key
HBIN045566_35879990
Pubmed Id
35879990
Doi
10.1155/2022/4135752
Paper Title
Taurine Ameliorates Iron Overload-Induced Hepatocyte Injury via the Bcl-2/VDAC1-Mediated Mitochondrial Apoptosis Pathway
Paper 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.
Journal
Oxid Med Cell Longev
Publish Year
2022
Experiment Subject
Experiment Type
Cell Experiment
Phenotype Related
Liver Injury
Paper Title Cn
Paper Title En
Taurine Ameliorates Iron Overload-Induced Hepatocyte Injury via the Bcl-2/VDAC1-Mediated Mitochondrial Apoptosis Pathway
Bilingual Status
semi_complete