title: Alternate-day fasting protects the rat heart against age-induced inflammation and fibrosis by inhibiting oxidative damage and NF-kB activation.
abstract: The free radical theory of aging is currently one of the most popular. In parallel, many studies have demonstrated the association of fibrosis and increased oxidative stress in the pathogenesis of some chronic human diseases, and fibrosis is often characteristic of aging tissues. One of the few interventions that effectively slow aging is calorie restriction and the protection against the age-associated increase of oxidative stress remains one of the foremost hypotheses to explain this action. As an alternative to traditional calorie restriction, another dietary regimen, termed alternate-day fasting, has also been tested, whose antiaging mechanisms have not been explored so much extensively. We thus studied the effects of alternate-day fasting, started at 2 months of age, on oxidative stress and fibrosis in the heart during aging. In the left ventricle of the heart of elderly (aged 24 months) versus young (aged 6 months) male rats we found a significant increase in oxidative stress paralleled by increased fibrosis. In parallel there was a significant increase in inflammatory cytokine levels and in NF-kB DNA binding activity with advancing age. Alternate-day fasting protected against all these age-related phenomena. These data support the hypothesis that this kind of dietary restriction protects against age-related fibrosis, at least in part by reducing inflammation and oxidative damage, and this protection can thus be considered a factor in the prevention of age-related diseases with sclerotic evolution.
authors.affiliation: Department of Clinical and Biological Sciences, University of Torino, Regione Gonzole 10, 10043 Orbassano, (TO), Italy. laura.castello@unito.it
authors.forename: Laura
authors.initials: L
authors.lastname: Castello
authors.forename: Teresa
authors.initials: T
authors.lastname: Froio
authors.forename: Marco
authors.initials: M
authors.lastname: Maina
authors.forename: Gabriella
authors.initials: G
authors.lastname: Cavallini
authors.forename: Fiorella
authors.initials: F
authors.lastname: Biasi
authors.forename: Gabriella
authors.initials: G
authors.lastname: Leonarduzzi
authors.forename: Alessio
authors.initials: A
authors.lastname: Donati
authors.forename: Ettore
authors.initials: E
authors.lastname: Bergamini
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Poli
authors.forename: Elena
authors.initials: E
authors.lastname: Chiarpotto
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D016207:Cytokines / Q000276:immunology; D005215:Fasting / Q000502:physiology*; D005355:Fibrosis / Q000517:prevention & control; D006321:Heart; D007249:Inflammation / Q000517:prevention & control; D008297:Male; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology*; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D016207:Cytokines; D016328:NF-kappa B