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Dietary quercetin supplementation alleviates disease related muscle injury in dystrophic muscle
Author(s) -
Hollinger Katrin,
Snella Elizabeth,
Shanely R. Andrew,
Selsby Joshua T.
Publication year - 2012
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.26.1_supplement.255.4
Subject(s) - fibrosis , myocyte , medicine , muscular dystrophy , duchenne muscular dystrophy , endocrinology , muscle hypertrophy , quercetin , biology , biochemistry , antioxidant
Duchenne muscular dystrophy is the most common, fatal, X‐linked muscle disease and is modeled by the mdx mouse. Dystrophic muscle shows signs of progressive necrosis and fibrosis leading to a loss of muscle function. Peroxisome proliferator‐activated receptor γ coactivator‐1α (PGC‐1α) up‐regulation has been shown to alleviate some aspects of dystrophic pathology. Quercetin (QCN), a natural polyphenolic compound derived from foods such as red apples and red onions, is a potent sirtuin 1 (SIRT1) activator capable of entering muscle cells via oral delivery. SIRT1, in turn, activates PGC‐1α by deacetylation. To determine the extent to which a diet containing QCN could alter the progression of disease related muscle injury 3 mo old mdx mice were fed a diet containing 0% or 0.2% QCN for 6 mo, sacrificed, and diaphragms removed. Control and treated mice ate similar amounts of food and grew at a similar rate during the study period. Dietary QCN reduced the number of extracellular nuclei/mm 2 by 37% (p<0.05). The number of muscle cells/mm 2 was increased by 20% (p<0.05) and muscle cells with centralized nuclei were reduced by 33% (p<0.05) in diaphragms from treated animals compared to control. Fibrosis was similar between groups. These data suggest that dietary QCN is beneficial to dystrophic muscle and warrants greater exploration as a potential therapeutic agent. Partially supported by the Martin Fund.