Red wine and equivalent oral pharmacological doses of resveratrol delay vascular aging but do not extend life span in rats
Carregando...
Citações na Scopus
65
Tipo de produção
article
Data de publicação
2012
Título da Revista
ISSN da Revista
Título do Volume
Editora
ELSEVIER IRELAND LTD
Autores
Citação
ATHEROSCLEROSIS, v.224, n.1, p.136-142, 2012
Resumo
Objective: To investigate, in male Wistar rats, the effects of long-term moderate red wine (RW) consumption (equivalent to similar to 0.15 mg% resveratrol RS), or RS in low (L, 0.15 mg%) or high (H, 400 mg%) doses in chow. Background: Both RW and RS exhibit cardioprotection. RS extends lifespan in obese rats. It is unclear whether RW consumption or low-dose RS delay vascular aging and prolong life span in the absence of overt risk factors. Methods: Endpoints were aerobic performance, exercise capacity, aging biomarkers (p53,p16,p21, telomere length and telomerase activity in aortic homogenates), vascular reactivity. Data were compared with controls (C) given regular chow. Results: Expressions of p53 decreased similar to 50% similar to with RW and LRS (p < 0.05 vs. C), p16 by similar to 29% with RW (p < 0.05 vs. C) and p21 was unaltered. RW and LRS increased telomere length >6.5-fold vs. C, and telomerase activity increased with LRS and HRS. All treatments increased aerobic capacity (C 32.5 +/- 1.2, RW 38.7 + 1.7, LRS 38.5 + 1.6, HRS 38.3 + 1.8 mlO2 min(-1) kg(-1)), and RW or LRS also improved time of exercise tolerance vs. C (p < 0.05). Endothelium-dependent relaxation improved with all treatments vs. C. Life span, however, was unaltered with each treatment vs. C = 673 +/- 30 days, p = NS. Conclusions: RW and LRS can preserve vascular function indexes in normal rats, although not extending life span. These effects were translated into better aerobic performance and exercise capacity.
Palavras-chave
Aging, Senescence, Polyphenols, Vascular aging, p53, p16, Red wine, Resveratrol
Referências
- Barger JL, 2003, EXP GERONTOL, V38, P1343, DOI 10.1016/j.exger.2003.10.017
- Barger JL, 2008, PLOS ONE, V3, P2264
- Baur JA, 2006, NATURE, V444, P337, DOI 10.1038/nature05354
- Baur JA, 2006, NAT REV DRUG DISCOV, V5, P493, DOI 10.1038/nrd2060
- Campisi J, 2005, CELL, V120, P513, DOI 10.1016/j.cell.2005.02.003
- CELERMAJER DS, 1994, J AM COLL CARDIOL, V24, P471
- Coimbra SR, 2005, BRAZ J MED BIOL RES, V38, P1339, DOI 10.1590/S0100-879X2005000900008
- Collins K, 2006, NAT REV MOL CELL BIO, V7, P484, DOI 10.1038/nrm1961
- Colman RJ, 2009, SCIENCE, V325, P201, DOI 10.1126/science.1173635
- da Luz PL, 1999, EXP MOL PATHOL, V65, P150, DOI 10.1016/S0014-4800(99)80004-5
- RENAUD S, 1992, LANCET, V339, P1523, DOI 10.1016/0140-6736(92)91277-F
- de Lange T, 2005, GENE DEV, V19, P2100, DOI 10.1101/gad.1346005
- Donehower LA, 2002, J CELL PHYSIOL, V192, P23, DOI 10.1002/jcp.10104
- Gourbunova V, 2003, J BIOL CHEM, V278, P7692
- Guarente L, 2011, NEW ENGL J MED, V364, P2235, DOI 10.1056/NEJMra1100831
- Heiss C, 2010, J AM COLL CARDIOL, V56, P218, DOI 10.1016/j.jacc.2010.03.039
- Holdt LM, 2011, ATHEROSCLEROSIS, V214, P264, DOI 10.1016/j.atherosclerosis.2010.06.029
- Howitz KT, 2003, NATURE, V425, P191, DOI 10.1038/nature01960
- Huang PH, 2010, ARTERIOSCL THROM VAS, V30, P869, DOI 10.1161/ATVBAHA.109.200618
- Kletsas D, 2004, ANN NY ACAD SCI, V1019, P330, DOI 10.1196/annals.1297.056
- Lagouge M, 2006, CELL, V127, P1109, DOI 10.1016/j.cell.2006.11.013
- Lang RM, 2005, J AM SOC ECHOCARDIOG, V18, P1440, DOI 10.1016/j.echo.2005.10.005
- Minamino T, 2007, CIRC RES, V100, P15, DOI 10.1161/01.RES.0000256837.40544.4a
- Minamino T, 2002, CIRCULATION, V105, P1541, DOI 10.1161/01.CIR.0000013836.85741.17
- Pearson KJ, 2008, CELL METAB, V8, P157, DOI 10.1016/j.cmet.2008.06.011
- Serrano AL, 2004, CIRC RES, V94, P575, DOI 10.1161/01.RES.0000122141.18795.9C
- Shain E, 2011, NATURE, V470, P359
- Majerska J, 2011, MOL BIOSYST, V7, P1013, DOI 10.1039/c0mb00268b
- Tyner SD, 2002, NATURE, V415, P45, DOI 10.1038/415045a
- Walter A, 2010, FASEB J, V24, P3360, DOI 10.1096/fj.09-149419