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Resveratrol Preserves Mitochondrial Function, Stimulates Mitochondrial Biogenesis, and Attenuates Oxidative Stress in Regulatory T Cells of Mice Fed a High‐Fat Diet
Author(s) -
Wang Bin,
Sun Jin,
Ma Yuhua,
Wu Guirong,
Tian Yingjie,
Shi Yonghui,
Le Guowei
Publication year - 2014
Publication title -
journal of food science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 150
eISSN - 1750-3841
pISSN - 0022-1147
DOI - 10.1111/1750-3841.12555
Subject(s) - resveratrol , mitochondrial biogenesis , oxidative stress , mitochondrion , reactive oxygen species , apoptosis , microbiology and biotechnology , chemistry , biogenesis , oxidative phosphorylation , mitochondrial ros , biology , pharmacology , biochemistry , gene
Consumption of high‐fat diet (HFD) is related with increased oxidative stress and dysfunctional mitochondria in many organs. The effects of resveratrol (trans‐3,5,4′‐trihydroxystilbene) that can protect T lymphocytes in various disease conditions on the HFD‐induced apoptosis of CD4 + CD25 + CD127 low/− regulatory T cells (Tregs) were studied, and the possible mechanism was postulated. Resveratrol significantly decreased Tregs death induced by 20‐wk HFD, being associated with the reduction of reactive oxygen species production and the alleviation of HFD‐induced loss of mitochondrial membrane potential (Δψm) in Tregs. Furthermore, resveratrol increased the expression of factors that regulated mitochondrial biogenesis in Tregs. Finally, resveratrol recovered the HFD‐induced activation of apoptotic markers in Tregs. Resveratrol protected Tregs against HFD‐induced apoptosis by reducing oxidative stress, restoring mitochondrial functional activities, and stimulating mitochondrial biogenesis.