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

Aldo Moreno-Ulloa, Leonardo Nogueira, Alonso Rodriguez, Jonathan Barboza, Michael C. Hogan, Guillermo Ceballos, Francisco Villarreal, Israel Ramirez-Sanchez

Research output: Contribution to journalArticlepeer-review

74 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)1370-1378
Number of pages9
JournalJournals of Gerontology - Series A Biological Sciences and Medical Sciences
Volume70
Issue number11
DOIs
StatePublished - Nov 2015

Keywords

  • (-)-Epicatechin
  • Mitochondrial biogenesis
  • Oxidative stress
  • Senescence-associated β-galactosidase

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