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Alpha‐Lipoic Acid Inhibits IL‐8 Expression by Reducing Oxidative Stress in Ataxia Telangiectasia Fibroblasts
Author(s) -
Yoon Jungyun,
Lim Joo Weon,
Kim Hyeyoung
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb426
Subject(s) - ataxia telangiectasia , alpha lipoic acid , reactive oxygen species , oxidative stress , microbiology and biotechnology , lipoic acid , mitochondrial ros , chemistry , apoptosis , mitochondrion , biology , biochemistry , dna damage , antioxidant , dna
Ataxia telangiectasia (A‐T) is a neurodegenerative and inherited disease caused by a mutation in the ataxia telangiectasia mutated (ATM) gene. ATM gene is associated with cell cycle arrest, DNA repair, or apoptosis. Reactive oxygen species (ROS) levels were higher in AT cells lacking ATM gene than in normal cells. Previously, we demonstrated that alpha‐lipoic acid inhibits IL‐1 beta‐induced IL‐8 expression by suppressing ROS production in A‐T fibroblasts. Ataxia telangiectasia (A‐T) fibroblasts were treated with or without alpha‐lipoic acid dissolved in ethanol (final concentration of 10 and 20 microM). ROS levels were determined using DCF‐DA. IL‐8 mRNA expression was determined by quantitative real‐time PCR. Mitochondrial functions such as oxygen consumption (OCR) and ATP production were assessed using Seahorse XF assay. Mitochondria membrane potential (MMP, Δ ψ m) was determined by measuring JC‐1 fluorescent dye using laser‐scanning confocal microscope. As a result, IL‐1 beta increased ROS levels and induced IL‐8 expression, but decreased mitochondrial functions in A‐T cells. IL‐1 beta‐induced IL‐8 expression and ROS production were inhibited by alpha‐lipoic acid. IL‐1 beta‐induced decrease in mitochondrial function (determined by OCR, ATP production, MMP) was reversed by alpha‐lipoic acid in A‐T cells. In conclusion, consumption of alpha‐lipoic acid‐containing foods may be beneficial for preventing inflammation of A‐T patients.