Abstract
Epidemiological evidence indicates that nutritionally-derived polyphenols such as resveratrol (RES) have neuroprotective properties. Administration of RES to culture media protects a wide variety of neuronal cell types from stress-induced death. Dietary supplementation of RES can ameliorate neuronal damage and death resulting from both acute and chronic stresses in rodents. The specific molecular mechanisms by which RES acts at the cellular level remain incompletely understood. However, many experimental data indicate that RES reduces or prevents the occurrence of oxidative damage. Here we discuss possible mechanisms by which RES might exert protection against oxidative damage and cell death. Evidence suggesting that RES’s chemical antioxidant potential is not sufficient explanation for its effects is discussed. Putative biological activities, including interactions with estrogen receptors and sirtuins are critically discussed. We provide a synthesis of how RES’s phytoestrogenic properties might mediate the neuronal stress resistance underlying its observed neuroprotective properties.
Highlights
The efficacy of nutritionally derived compounds as neuroprotective agents is increasingly supported by empirical evidence
Mattson et al hypothesized that MnSOD induction protects hippocampal neurons from oxidative stress induced apoptosis in vitro by reducing membrane peroxidation [48]
Transgenic mice that overexpress human MnSOD are protected from oxidative damage and neuron loss induced by ischemia and the neurotoxin MPTP [44]
Summary
The efficacy of nutritionally derived compounds as neuroprotective agents is increasingly supported by empirical evidence. Polyphenols are small molecule antioxidants that are hypothesized to offer protection against the negative effects of oxidative stress in many tissues including brain, and this may underlie their ability to protect against cell death. An alternative to direct chemical interactions is the possibility that RES and related polyphenols work to enhance endogenous intracellular defense systems and in turn protect against cellular stress, dysfunction and death. We begin this review by first summarizing the literature supporting the neuroprotective actions of RES, followed by a critical review of recent findings regarding putative mechanisms of RES’s actions at the cellular level. We extend this discussion to dietary delivery strategies that may increase.
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