Sirt1/PGC-1

Rasouri, Soumya; Lagouge, Marie; Auwerx, Johan

doi:10.1051/medsci/20072310840

Cited by 22 publications

(7 citation statements)

References 31 publications

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“…The physiological significance of PGC-1 in mitochondrial energy metabolism has been well demonstrated [12], [13]. Several groups including our studies have demonstrated that PGC-1α exerted neuroprotective effects in multiple neurological diseases [14], [15], [16], [17]. An intriguing finding in these studies was that PGC-1α null mice developed spongiform neurodegeneration in selective brain areas, which indicated the direct role of PGC-1α in the neurodegeneration [13].…”

Section: Introductionsupporting

confidence: 56%

Diammonium Glycyrrhizinate Upregulates PGC-1α and Protects against Aβ1–42-Induced Neurotoxicity

Zhu

Chen

et al. 2012

PLoS ONE

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Mitochondrial dysfunction is a hallmark of beta-amyloid (Aβ)-induced neurotoxicity in Alzheimer's disease (AD), and is considered an early event in AD pathology. Diammonium glycyrrhizinate (DG), the salt form of Glycyrrhizin, is known for its anti-inflammatory effects, resistance to biologic oxidation and membranous protection. In the present study, the neuroprotective effects of DG on Aβ1–42-induced toxicity and its potential mechanisms in primary cortical neurons were investigated. Exposure of neurons to 2 µM Aβ1–42 resulted in significant viability loss and cell apoptosis. Accumulation of reactive oxygen species (ROS), decreased mitochondrial membrane potential, and activation of caspase-9 and caspase-3 were also observed after Aβ1–42 exposure. All these effects induced by Aβ1–42 were markedly reversed by DG treatment. In addition, DG could alleviate lipid peroxidation and partially restore the mitochondrial function in Aβ1–42-induced AD mice. DG also significantly increased the PGC-1α expression in vivo and in vitro, while knocking down PGC-1α partially blocked the protective effects, which indicated that PGC-1α contributed to the neuroprotective effects of DG. Furthermore, DG significantly decreased the escape latency and search distance and increased the target crossing times of Aβ1–42-induced AD mice in the Morris water maze test. Therefore, these results demonstrated that DG could attenuate Aβ1–42-induced neuronal injury by preventing mitochondrial dysfunction and oxidative stress and improved cognitive impairment in Aβ1–42-induced AD mice, indicating that DG exerted potential beneficial effects on AD.

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Section: Introductionsupporting

confidence: 56%

Diammonium Glycyrrhizinate Upregulates PGC-1α and Protects against Aβ1–42-Induced Neurotoxicity

Zhu

Chen

et al. 2012

PLoS ONE

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“…SIRT1 can also regulate oxidative stress by modulating FOXO3, which regulates expression of antioxidant genes, such as MnSOD [158]. It is also notable that SIRT1 can regulate cellular redox status by modulating mitochondrial biogenesis by inducing PGC1-α and nitric oxide synthase [156,159]. Oxidative stress is known to suppress expression and activity of SIRT1 at the transcriptional and posttranslational levels [14,156].…”

Section: A Potential Mechanistic Link Between Dietary Restriction mentioning

confidence: 99%

Dietary Restriction and Neuroinflammation: A Potential Mechanistic Link

Bok

Lee

et al. 2019

IJMS

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Chronic neuroinflammation is a common feature of the aged brain, and its association with the major neurodegenerative changes involved in cognitive impairment and motor dysfunction is well established. One of the most potent antiaging interventions tested so far is dietary restriction (DR), which extends the lifespan in various organisms. Microglia and astrocytes are two major types of glial cells involved in the regulation of neuroinflammation. Accumulating evidence suggests that the age-related proinflammatory activation of astrocytes and microglia is attenuated under DR. However, the molecular mechanisms underlying DR-mediated regulation of neuroinflammation are not well understood. Here, we review the current understanding of the effects of DR on neuroinflammation and suggest an underlying mechanistic link between DR and neuroinflammation that may provide novel insights into the role of DR in aging and age-associated brain disorders.

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“…However, recent studies started to reveal the ability for resveratrol to exert neuroprotective effects through activation of SIRT1 and production of vitagenes [79]. Resveratrol was shown to confer special effects in increasing the lifespan of Saccharomyces cerevisiae [80], and this effect was attributed to its ability to activate sirtuins, which belong to a conserved family of NAD + -dependent deacetylases [66].…”

Section: Oxidative Stress and Neurodegenerative Disordersmentioning

confidence: 99%

Resveratrol as a Therapeutic Agent for Neurodegenerative Diseases

et al. 2010

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Excess production of reactive oxygen species in the brain has been implicated as a common underlying risk factor for the pathogenesis of a number of neurodegenerative disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and stroke. In recent years, there is considerable interest concerning investigation of antioxidative and anti-inflammatory effects of phenolic compounds from different botanical sources. In this review, we first describe oxidative mechanisms associated with stroke, AD, and PD, and subsequently, we place emphasis on recent studies implicating neuroprotective effects of resveratrol, a polyphenolic compound derived from grapes and red wine. These studies show that the beneficial effects of resveratrol are not only limited to its antioxidant and anti-inflammatory action but also include activation of sirtuin 1 (SIRT1) and vitagenes, which can prevent the deleterious effects triggered by oxidative stress. In fact, SIRT1 activation by resveratrol is gaining importance in the development of innovative treatment strategies for stroke and other neurodegenerative disorders. The goal here is to provide a better understanding of the mode of action of resveratrol and its possible use as a potential therapeutic agent to ameliorate stroke damage as well as other age-related neurodegenerative disorders.

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Sirt1/PGC-1

Cited by 22 publications

References 31 publications

Diammonium Glycyrrhizinate Upregulates PGC-1α and Protects against Aβ1–42-Induced Neurotoxicity

Diammonium Glycyrrhizinate Upregulates PGC-1α and Protects against Aβ1–42-Induced Neurotoxicity

Dietary Restriction and Neuroinflammation: A Potential Mechanistic Link

Resveratrol as a Therapeutic Agent for Neurodegenerative Diseases

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