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Review
. 2006;13(9):989-96.
doi: 10.2174/092986706776360987.

"V体育官网" Vascular dysfunction in aging: potential effects of resveratrol, an anti-inflammatory phytoestrogen

Nazar Labinskyy  1 , Anna Csiszar, Gabor Veress, Gyorgyi Stef, Pal Pacher, Gabor Oroszi, Joseph Wu, Zoltan Ungvari
Affiliations
Review

Vascular dysfunction in aging: potential effects of resveratrol, an anti-inflammatory phytoestrogen

Nazar Labinskyy (V体育2025版) et al. Curr Med Chem. 2006.

Abstract

Epidemiological studies demonstrated that even in the absence of other risk factors (e. g. diabetes, hypertension, hyperhomocysteinemia, hypercholesterolemia), advanced age itself significantly increases cardiovascular morbidity by enhancing vascular oxidative stress and inflammation. Because the population in the Western world is rapidly aging, there is a substantial need for pharmacological interventions that delay the functional decline of the cardiovascular system. Resveratrol is an atoxic phytoestrogen found in more than 70 plants including grapevine and berries. Recent data suggest that nutritional intake of resveratrol and other polyphenol compounds may contribute to the "French paradox", the unexpectedly low cardiovascular morbidity in the Mediterranean population. There is increasing evidence that resveratrol exerts multifaceted anti-oxidant and/or anti-inflammatory effects in various disease models. Importantly, resveratrol was reported to slow aging and increase lifespan in simple organisms and has been suggested as a potential calorie restriction mimetic. Resveratrol has also been reported to activate NAD-dependent histone deacetylases (sirtuins), which may contribute to its anti-aging effects VSports手机版. This review focuses on the role of oxidative stress and inflammation in cardiovascular dysfunction in aging, and on emerging anti-aging therapeutic strategies offered by resveratrol and other polyphenol compounds. .

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Figures

Fig. 1
Fig. 1
Chemical structure of resveratrol (trans–3, 4′, 5–trihydroxystilbene) and other dietary polyphenols.
Fig. 2
Fig. 2
Original recordings showing ADP-, epinephrine- and collagen-induced aggregation in platelets of high risk human cardiac patients. B: Resveratrol significantly inhibits collagen- and epinephrine-induced aggregation, whereas it exerts a less pronounced effect on ADP-induced aggregation (optical aggregometry).
Fig. 3
Fig. 3
Resveratrol-induced dilations of isolated, perfused small mesenteric arteries (d: ~300 μm) of young (3 month old) and aged (29 month old) male F344 rats. B: Effect of resveratrol pretreatment (10−6 mol/L, for 30 min) on acetylcholine-induced dilations of young and aged arteries. The inner vascular diameter was measured by videomicroscopy as described [–98]. The TXA2 mimetic U46619 (10−7 mol/L) was used for preconstriction. Data are mean±S.E.M. *p<0.05
Fig. 4
Fig. 4
Superoxide production in cultured carotid arteries of 29 month old male F344 rats with or without resveratrol incubation (24 h, in sterile vessel culture; for a description of the technique see references [53, 87, 99, 100]). Data are mean ± S.E.M. (n=5–8 for each group). B–D: Fluorescent photomicrographs showing that compared to young vessels (B), there was a significantly increased O2·− production in the endothelial (arrows) and smooth muscle cells of aged arteries (C), as indicated by the intensive red fluorescent staining of the nuclei by ethidium bromide. The number and staining intensity of ethidium bromide-positive endothelial nuclei in aged vessels were not significantly decreased by short-term treatment with resveratrol (D). Green autofluorescence is shown for orientation purposes. Images are representative to 6 independent experiments.
Fig. 5
Fig. 5
Expression of iNOS (A) and ICAM-1 (B) mRNA in cultured carotid arteries of 29 month old male F344 rats with or without resveratrol incubation (24 h, in sterile vessel culture; for a description of the technique see references [53, 87, 99, 100]). Quantification of mRNA expression was performed by real-time PCR, as described [53, 87, 99, 100]. C: Expression of ICAM-1 mRNA in carotid arteries of 29 month old male F344 rats with or without resveratrol treatment (p.o. 3 mg/kg/day, for 1 week). Data are mean ± S.E.M. (n=5 for each group).
Fig. 6
Fig. 6
Proposed scheme for the mechanisms by which aging promotes oxidative stress, endothelial dysfunction and pro-inflammatory phenotypic alterations in blood vessels. The model predicts that aging is associated with an increased ROS generation by NAD(P)H oxidase and/or mitochondrial sources, which activates redox-sensitive transcription factors (NF-κB) upregulating inflammatory gene expression. The resulting pro-inflammatory phenotype of arteries will promote atherogenesis, especially if other risk factors (e.g. hypertension, hyperhomocysteinemia, hypercholesterolemia) are also present. We propose that resveratrol inhibits the ROS - NF-κB axis, inhibits platelet activation, increases NO bioavailability and/or activates sirtuins thereby helps to maintain a youthful vascular phenotype. It is likely that inhibition of PARP-1 will increase NAD+ levels, which serves as a co-factor for sirtuin activation. Thus, it can be predicted that resveratrol and PARP inhibitors exert additive anti-aging actions.
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