Neuroprotective abilities of resveratrol and other red wine constituents against nitric oxide‐related toxicity in cultured hippocampal neurons

Bastianetto, Stéphane; Zheng, Wenhua; Quirion, Rémi

doi:10.1038/sj.bjp.0703626

Cited by 275 publications

(168 citation statements)

References 57 publications

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“…Previous studies showed that LA treatment counteracts an arsenic-induced decrease in GSH levels in several brain regions (Shila et al, 2005), and that EGCG protects PC12 cells against the effects of serum withdrawal (Reznichenko et al, 2005) and oxidative stress (Koh etal., 2003). In addition, resveratrol prevents NO-related toxicity (Bastianetto et al, 2000) in hippocampal neurons and curcumin blocks toxicity from the Alzheimer's disease related Aβ42 oligomer in neuroblastoma cells (Yang et al, 2005). Moreover, melatonin prevents H 2 O 2 activation of the pro-apoptotic enzyme, caspase-3 (Juknat et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Antioxidants prevent ethanol-associated apoptosis in fetal rhombencephalic neurons

Antonio

Druse

2008

Brain Research

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It is well known that ethanol damages the developing nervous system by augmenting apoptosis. Previously, this laboratory reported that ethanol augments apoptosis in fetal rhombencephalic neurons, and that the increased apoptosis is associated with reduced activity of the phosphatidylinositol 3'kinase pathway and downstream expression of pro-survival genes. Other laboratories have shown that another mechanism by which ethanol induces apoptosis in developing neurons is through the generation of reactive oxygen species (ROS) and the associated oxidative stress.The present study used an in vitro model to investigate the potential neuroprotective effects of several antioxidants against ethanol-associated apoptosis in fetal rhombencephalic neurons. The investigated antioxidants included three phenolics: (-)-epigallocatechin-3-gallate (EGCG), a flavanoid polyphenol found in green tea; curcumin, found in tumeric; and resveratrol (3,5,4'-trihydroxystilbene), a component of red wine. Additional antioxidants, including melatonin, a naturally occurring indole, and α-lipoic acid, a naturally occurring dithiol, were also investigated.These studies demonstrated that a 24-hour treatment of fetal rhombencephalic neurons with 75 mM ethanol caused a 3-fold increase in the percentage of apoptotic neurons. However, co-treatment of these cultures with any of the five different antioxidants prevented ethanol-associated apoptosis. Antioxidant treatment did not alter the extent of apoptosis in control neurons, i.e., those cultured in the absence of ethanol. These studies showed that several classes of antioxidants can exert neuroprotection against ethanol-associated apoptosis in fetal rhombencephalic neurons.

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Section: Discussionmentioning

confidence: 99%

Antioxidants prevent ethanol-associated apoptosis in fetal rhombencephalic neurons

Antonio

Druse

2008

Brain Research

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“…However, the actions of flavonoids are complex and often seemingly antagonistic or paradoxical. For example, while flavonoids are described as antioxidant agents protecting against oxidative insults to cells and apoptosis [11,13,88], others have found flavonoids to be pro-oxidants and -apoptotic [33,212,221]. Thus, it becomes clear that the effects of flavonoids depend on different factors such as the specific compound used, the cell type, concentrations, experimental design, and the general context in which flavonoids are used.…”

Section: Biological and Cellular Propertiesmentioning

confidence: 99%

“…Other lines of research focused on the binding of flavonoids such as apigenin, naringenin, kaempferol, quercetin-3-O-glucoside and others to benzodiazepine binding sites [149] of different receptors including the GABA-A-receptor [52,132] and adenosine receptors [139], and investigated their anxiolytic potential [149] as a possible mechanism of action in the CNS. Bastianetto et al report that antioxidant effects are not the only mechanism of flavonoid-mediated protection against neuronal death and show attenuation of NO • -induced activation of protein kinase C (PKC) by G. biloba [12] and resveratrol [13] to be partially involved in the protection against neurotoxicity.…”

Section: Flavonoids: Neuroprotective Agents In Vivo and In Vitro?mentioning

confidence: 99%

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

Schroeter

Boyd

Spencer

et al. 2002

Neurobiology of Aging

302

178

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Oxidative and nitrosative stress is increasingly associated with the pathology of neurodegeneration and aging. The molecular mechanisms underlying oxidative/nitrosative stress-induced neuronal damage are emerging and appear to involve a mode of death in which mitogen-activated protein kinase (MAPK) signaling pathways are strongly implicated. Thus, attention is turning towards the modulation of intracellular signaling as a therapeutic approach against neurodegeneration. Both endogenous and dietary agents have been suggested as potent modulators of intracellular signal transduction, e.g. nitric oxide and flavonoids, respectively. This review addresses recent findings on the biological effects of flavonoids and nitric oxide in neurodegeneration and aims to elucidate the rationale for their prospective use as modulators of cellular signal transduction. © 2002 Elsevier Science Inc. All rights reserved.Keywords: Apoptosis; Oxidative stress; Neuron; Flavonoids; MAP kinase; JNK; ERK; Epicatechin; Nitric oxide; Mitochondria; Redox status; Polyphenols Abbreviations: AKT, serine/threonine kinase (also known as protein kinase B); AP-1, activator protein-1; Apaf-1, apoptosis protease activating factor-1; ASK1, apoptosis signal-regulating kinase-1; Bad, Bcl-2/BclX Lassociated death promoting protein; Bax, pro-apoptotic protein of the Bcl-2 family; Bcl-2, B-cell lymphoma 2: protein with anti-apoptotic properties; BclX L , long form of Bclx: anti-apoptotic protein of the Bcl-2 family; Caspase, cysteinyl aspartic acid-protease; c-Jun, mammalian equivalent of Jun: part of the AP-1 transcription complex; CREB, cAMP response element binding protein; DIABLO/smac, mitochondria-related pro-apoptotic protein: inhibits XIAP; ERK1/2, extracellular signal-related kinase; Fas, CD95: member of the TNF receptor family; GSHST, glutathione Stransferase; JNK, c-Jun amino-terminal kinase; MAPK, mitogen-activated protein kinase; MAPKK, MAPK kinase; MAPKKK, MAPKK kinase; MEK1/2, ERK1/2-specific MAPKK; MKK4/7, JNK-specific MAPKK; MSK1, mitogen-and stress-activated kinase-1; NF-B, nuclear factor of immunoglobulin k locus in B-cells; ONOO − , peroxynitrite anion; p53, pro-apoptotic tumor suppressor gene product; PI3-kinase, phosphoinositol 3-kinase; Ras, small G-protein; RNS, reactive nitrogen species; ROS, reactive oxygen species; RSK, pp90 ribosomal S6 kinase; SAPK, stressactivated protein kinase; XIAP, X-linked inhibitor of apoptosis: inhibits the activation of caspase-9

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“…Administration of resveratrol to rats reduced ischemic damage to the brain in a model of stroke (Huang et al, 2001) and also protected spinal cord neurons against ischemic injury (Kaplan et al, 2005). Resveratrol can protect cultured neurons against nitric oxide-mediated oxidative stress-induced death (Bastianetto et al, 2000). Similarly, resveratrol protected dopaminergic neurons in midbrain slice cultures against metabolic and oxidative insults, a model relevant to Parkinson's disease (Okawara et al, 2007).…”

Section: Subtoxic Doses Of Phytochemicals Can Protect Neurons Againstmentioning

confidence: 99%

Viewpoint: Mechanisms of Action and Therapeutic Potential of Neurohormetic Phytochemicals

Mattson¹,

Son²,

Camandola³

2007

Dose-Response

124

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ᮀ The nervous system is of fundamental importance in the adaptive (hormesis) responses of organisms to all types of stress, including environmental "toxins". Phytochemicals present in vegetables and fruits are believed to reduce the risk of several major diseases including cardiovascular disease, cancers and neurodegenerative disorders. Although antioxidant properties have been suggested as the basis of health benefits of phytochemicals, emerging findings suggest a quite different mechanism of action. Many phytochemicals normally function as toxins that protect the plants against insects and other damaging organisms. However, at the relatively low doses consumed by humans and other mammals these same "toxic" phytochemicals activate adaptive cellular stress response pathways that can protect the cells against a variety of adverse conditions. Recent findings have elucidated hormetic mechanisms of action of phytochemicals (e.g., resveratrol, curcumin, sulforaphanes and catechins) using cell culture and animal models of neurological disorders. Examples of hormesis pathways activated by phytochemicals include the transcription factor Nrf-2 which activates genes controlled by the antioxidant response element, and histone deacetylases of the sirtuin family and FOXO transcription factors. Such hormetic pathways stimulate the production of antioxidant enzymes, protein chaperones and neurotrophic factors. In several cases neurohormetic phytochemicals have been shown to suppress the disease process in animal models relevant to neurodegenerative disorders such as Alzheimer's and Parkinson's diseases, and can also improve outcome following a stroke. We are currently screening a panel of biopesticides in order to establish hormetic doses, neuroprotective efficacy, mechanisms of action and therapeutic potential as dietary supplements.

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Neuroprotective abilities of resveratrol and other red wine constituents against nitric oxide‐related toxicity in cultured hippocampal neurons

Cited by 275 publications

References 57 publications

Antioxidants prevent ethanol-associated apoptosis in fetal rhombencephalic neurons

Antioxidants prevent ethanol-associated apoptosis in fetal rhombencephalic neurons

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

Viewpoint: Mechanisms of Action and Therapeutic Potential of Neurohormetic Phytochemicals

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