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

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

Author information

1
Department of Medicine, University of California, San Diego, La Jolla, California, USA . Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Mexico.
2
Instituto de Bioquímica Médica Leopoldo De Méis, CCS, UFRJ, Rio de Janeiro, Brazil.
3
Department of Medicine, University of California, San Diego, La Jolla, California, USA .
4
Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Mexico.
5
Department of Medicine, University of California, San Diego, La Jolla, California, USA . Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Mexico. israel.ramirez14@hotmail.com.

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.

KEYWORDS:

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

PMID:
25143004
PMCID:
PMC4715241
DOI:
10.1093/gerona/glu131
[Indexed for MEDLINE]
Free PMC Article

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