Recovery of Indicators of Mitochondrial Biogenesis, Oxidative Stress, and Aging With (-)-Epicatechin in Senile Mice

J Gerontol A Biol Sci Med Sci. 2015 Nov;70(11):1370-8. doi: 10.1093/gerona/glu131. Epub 2014 Aug 20.


There is evidence implicating oxidative stress (OS) as the cause of the deleterious effects of aging. In this study, we evaluated the capacity of the flavanol (-)-epicatechin (Epi) to reduce aging-induced OS and restore mitochondrial biogenesis, as well as, structural and functional endpoints in aged mice. Senile (S; 26-month-old) C57BL/6 male mice were randomly assigned to receive either water (vehicle) or 1mg/kg of Epi via oral gavage (twice daily) for 15 days. Young (Y; 6-month-old) mice were used as controls. In S brain, kidney, heart, and skeletal muscle (compared with Y animals) an increase in OS was observed as evidenced by increased protein-free carbonyls and decreased reduced glutathione levels as well as sirtuin 3, superoxide dismutase 2, catalase, thioredoxin and glutathione peroxidase protein levels. Well-recognized factors (eg, sirtuin 1) that regulate mitochondrial biogenesis and mitochondrial structure- and/or function-related endpoints (eg, mitofilin and citrate synthase) protein levels were also reduced in S organs. In contrast, the aging biomarker senescence-associated β-galactosidase was increased in S compared with Y animals, and Epi administration reduced levels towards those observed in Y animals. Altogether, these data suggest that Epi is capable of shifting the biology of S mice towards that of Y animals.

Keywords: (−)-Epicatechin; Mitochondrial biogenesis; Oxidative stress; Senescence-associated β-galactosidase..

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Age Factors
  • Aging / drug effects*
  • Aging / physiology*
  • Animals
  • Brain / metabolism
  • Brain / pathology
  • Catechin / pharmacology*
  • Citrate (si)-Synthase / metabolism
  • Kidney / metabolism
  • Kidney / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mitochondrial Proteins / metabolism
  • Muscle, Skeletal / metabolism
  • Muscle, Skeletal / pathology
  • Myocardium / metabolism
  • Myocardium / pathology
  • Organelle Biogenesis*
  • Oxidative Stress / drug effects*
  • Oxidative Stress / physiology*
  • Oxidoreductases / metabolism
  • beta-Galactosidase / metabolism


  • Mitochondrial Proteins
  • Catechin
  • Oxidoreductases
  • Citrate (si)-Synthase
  • beta-Galactosidase