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Effect of chronic dietary quercetin enrichment on cardiac function in dystrophic mice
Author(s) -
Ballmann Christopher,
Beyers Ronald,
Denney Thomas,
Selsby Joshua,
Quindry John
Publication year - 2015
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.29.1_supplement.1039.5
Subject(s) - cardiac function curve , quercetin , ejection fraction , medicine , duchenne muscular dystrophy , stroke volume , cardiology , endocrinology , heart failure , biology , antioxidant , biochemistry
In Duchenne muscular dystrophy (DMD), cardiac function declines with age and causes 40% of related deaths. New treatments are needed to treat cardiac pathologies related to DMD and preserve cardiac performance across the lifespan. Relative to DMD pathology, consumption of quercetin promotes anti‐inflammatory effects, activates PGC‐1α, up‐regulates endogenous antioxidants, and mitochondrial biogenesis. We investigated chronic 0.2% quercetin dietary enrichment as a strategy to attenuate cardiac function abnormalities in mdx mice. Mdx mice were randomly assigned to: 0.2% quercetin enriched (mdxQ) or control (mdx) diet for 12 months and compared to age matched, control fed C57 mice (n=8/group). Hearts received 7T MRI to quantify cardiac function at 2, 10, and 14 months of age. Reflective of aging, end diastolic volume increased at 14 months in all groups (p=0.001). Quercetin enrichment preserved calculated ejection fraction (p<0.001), stroke volume (p<0.001), fractional shortening (p=0.0013), systolic wall thickness (p=0.006) and cardiac output (p<0.001) at 10 and 14 months in mdxQ compared to mdx. Furthermore, quercetin attenuated increases in end systolic volume at 14 months (p<0.001) in mdx mice. Results confirm age‐dependent declines in cardiac function occur in mdx mice. Data also indicate that chronic quercetin enrichment prevented cardiac dysfunction in mdx mice. Additional experiments are needed to identify physiological mechanisms responsible for protection due to quercetin intake and optimize dosing strategies. Funded by: Duchenne Alliance