Resveratrol attenuates peripheral and brain inflammation and reduces ischemic brain injury in aged female mice

Jeong, Sae Im; Shin, Jeong-Ah; Cho, Sunghee; Kim, Hye Won; Lee, Ji Yoon; Kang, Jihee Lee; Park, Eun Mi

doi:10.1016/j.neurobiolaging.2016.04.007

Cited by 48 publications

(40 citation statements)

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“…Inflammasome activation can also be counteracted by resveratrol in liver of old mice . In aged female mice, resveratrol administration attenuated inflammation in visceral adipose tissue and in the brain and decreased peripheral inflammation and stroke‐induced brain injury . Resveratrol‐enriched rice has been shown to retard inflamm‐aging in dermal fibroblasts through controlling matrix metalloproteinase‐1 (MMP‐1)‐mediated ultraviolet B (UVB)‐induced skin aging, apoptosis‐induced skin aging, and inflammation in dermal .…”

Section: The Effect Of Resveratrol On Aging Biomarkersmentioning

confidence: 99%

Effect of resveratrol and pterostilbene on aging and longevity

2017

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Over the past years, several studies have found that foods rich in polyphenols protect against age-related disease, such as atherosclerosis, cardiovascular disease, cancer, arthritis, cataracts, osteoporosis, type 2 diabetes (T2D), hypertension and Alzheimer's disease. Resveratrol and pterostilbene, the polyphenol found in grape and blueberries, have beneficial effects as antiaging compounds through modulating the hallmarks of aging, including oxidative damage, inflammation, telomere attrition and cell senescence. In this review, we discuss the relationship between resveratrol and pterostilbene and possible aging biomarker, including oxidative stress, inflammation, and highcalorie diets. Moreover, we also discuss the positive effect of Abbreviations: ABTS, 2,2 0 -Azino-bis (3-ethylbenzothiazoline-6-sulfonic acid; Akt, v-akt murine thymoma viral oncogene; AMPK, AMP-activated kinase; ARE, antioxidant response element; C. elegans, Caenorhabditis elegans; cAMP, cyclic adenosine monophosphate; CCL3, C-C motif chemokine ligand 3; CNS, central nervous system; CREB, cAMP response element binding protein; CRP, c-reactive protein; DPPH, 2,2-diphenyl-1-picryl-hydrazyl; eNOS, endothelial nitric oxide synthase; ERK, extracellular-signal-regulated kinase; ER-a, estrogen receptor alpha; FOXO1, forkhead box protein O1; FOXO3, forkhead box O3A protein; GSH, glutathione; GSH-Px, glutathione peroxidase; GSK3b, glycogen synthase kinase 3 b; hTERT, human telomerase reverse transcriptase; HtrA2, HtrA serine peptidase 2; IDH2, dehydrogenase 2; IFN-c, interferon gamma; IL-18, interleukin-18; IL-1b, interleukin 1 b; IL-6, interleukin-6; LDL, low-density lipoprotein; LPS, lipopolysaccharides; MAPK, mitogen-activated protein kinase; MLC, myosin light chain; MMP-1, matrix metalloproteinase-1; MMP-2, matrix metalloproteinase-2; MMP-9, matrix metalloproteinase-9; MnSOD, manganese superoxide dismutase; mRNA, messenger RNA; mtROS, mitochondrial reactive oxygen species; NADPH, nicotinamide adenine dinucleotide phosphate; NALP-3, NACHT 5 LRR and PYD domainscontaining protein 3; NAMPT, nicotinamide phosphoribosyltransferase; NFAT, nuclear factor of activated T-cells; NF-rB, nuclear factor-jB; NO, nitric oxide; Nrf2, nuclear factor erythroid 2-related factor 2; NS, Nutritional Supplement; OA, osteoarthritis; oxoLDL, oxidized low-density lipoprotein; PARK7, Parkinson disease protein 7; PARKIN, parkinson juvenile disease protein; PGC-1a, peroxisome proliferator-activated receptor gamma coactivator 1-a; PINK1, PTEN-induced putative kinase 1; PKB, protein kinase B; RhoA, Ras homolog gene family 5 member A; ROCK2, Rho-associated 5 coiled-coil containing protein kinase 2; ROS, reactive oxygen species; SAMP8, senescence accelerated mouse-prone 8; SCID, severe combined immunodeficiency; SHR, spontaneously hypertensive rat; SIRT1, sirtuin 1; SIRT4, sirtuin 4; SOD, superoxide peroxidase; STZ, streptozotocin; T2D, type 2 diabetes; TIMP-1, TIMP metallopeptidase inhibitor 1; TLR5, toll-like receptor 5; TNF-a, tumor necrosis factor alpha; UVB, ultraviol...

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Section: The Effect Of Resveratrol On Aging Biomarkersmentioning

confidence: 99%

Effect of resveratrol and pterostilbene on aging and longevity

2017

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“…Recently, resveratrol has been suggested to have neuroprotective effects against many neurological diseases (Porro et al, 2015; Abdel-Aleem et al, 2016; Ghaiad et al, 2016; Jeong et al, 2016; Shi et al, 2016; Xu et al, 2017), and several underlying mechanisms for this effect have been suggested. For example, resveratrol attenuates hypoxia-induced neurotoxicity by inhibiting microglial activation (Zhang et al, 2015), and similarly constrains amyloid-β-induced microglial activation via NOX (Yao et al, 2015).…”

Section: Pharmacological Approaches For Modulating Microglial Phenotypesmentioning

confidence: 99%

Pharmacological Modulation of Functional Phenotypes of Microglia in Neurodegenerative Diseases

Song

Suk

2017

Front. Aging Neurosci.

140

112

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Microglia are the resident innate immune cells of the central nervous system that mediate brain homeostasis maintenance. Microglia-mediated neuroinflammation is a hallmark shared by various neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis. Numerous studies have shown microglial activation phenotypes to be heterogeneous; however, these microglial phenotypes can largely be categorized as being either M1 or M2 type. Although the specific classification of M1 and M2 functionally polarized microglia remains a topic for debate, the use of functional modulators of microglial phenotypes as potential therapeutic approaches for the treatment of neurodegenerative diseases has garnered considerable attention. This review discusses M1 and M2 microglial phenotypes and their relevance in neurodegenerative disease models, as described in recent literature. The modulation of microglial polarization toward the M2 phenotype may lead to development of future therapeutic and preventive strategies for neuroinflammatory and neurodegenerative diseases. Thus, we focus on recent studies of microglial polarization modulators, with a particular emphasis on the small-molecule compounds and their intracellular target proteins.

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“…Our lab and others have demonstrated the efficacy of preconditioning with resveratrol (resveratrol preconditioning, RPC), a naturally occurring polyphenolic compound 2, 3 . RPC-induced ischemic tolerance is observed at both early (24 hours) and late (>1 week) time points post-injury, with validation across species, age, sex and models of cerebral ischemia including neonatal hypoxia-ischemia, ischemic stroke, recurrent stroke and asphyxial cardiac arrest 3–6 . Yet, the molecular mechanism(s) of RPC are still unclear.…”

Section: Introductionmentioning

confidence: 98%

“…Resveratrol-induced protection has been attributed to the modulation of systemic processes, such as inflammation 6 and blood flow 7 , which then manifests in the brain. Still, resveratrol protects isolated neurons in culture 8 as well as organotypic cultures 9 , which have supporting cell types but lack circulation, demonstrating the existence of a brain-intrinsic response that is sufficient for ischemic tolerance.…”

Section: Introductionmentioning

confidence: 99%

Neuronal SIRT1 (Silent Information Regulator 2 Homologue 1) Regulates Glycolysis and Mediates Resveratrol-Induced Ischemic Tolerance

Koronowski

Khoury

Saul

et al. 2017

Stroke

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BACKGROUND AND PURPOSE Resveratrol, at least in part via Sirt1 activation, protects against cerebral ischemia when administered 2 days prior to injury. However, it remains unclear if Sirt1 activation must occur, and in which brain cell types, for the induction of neuroprotection. We hypothesized that neuronal Sirt1 is essential for resveratrol-induced ischemic tolerance and sought to characterize the metabolic pathways regulated by neuronal Sirt1 at the cellular level in the brain. METHODS We assessed infarct size and functional outcome following transient 60 minute middle cerebral artery occlusion in control and inducible, neuronal-specific Sirt1 knockout mice. Non-targeted primary metabolomics analysis identified putative Sirt1-regulated pathways in brain. Glycolytic function was evaluated in acute brain slices from adult mice and primary neuronal-enriched cultures under ischemic penumbra-like conditions. RESULTS Resveratrol-induced neuroprotection from stroke was lost in neuronal Sirt1 knockout mice. Metabolomics analysis revealed alterations in glucose metabolism upon deletion of neuronal Sirt1, accompanied by transcriptional changes in glucose metabolism machinery. Furthermore, glycolytic ATP production was impaired in acute brain slices from neuronal Sirt1 knockout mice. Conversely, resveratrol increased glycolytic rate in a Sirt1-dependent manner and under ischemic penumbra-like conditions in vitro. CONCLUSIONS Our data demonstrate that resveratrol requires neuronal Sirt1 to elicit ischemic tolerance and identify a novel role for Sirt1 in the regulation of glycolytic function in brain. Identification of robust neuroprotective mechanisms that underlie ischemia tolerance and the metabolic adaptations mediated by Sirt1 in brain are crucial for the translation of therapies in cerebral ischemia and other neurological disorders.

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Resveratrol attenuates peripheral and brain inflammation and reduces ischemic brain injury in aged female mice

Cited by 48 publications

References 44 publications

Effect of resveratrol and pterostilbene on aging and longevity

Effect of resveratrol and pterostilbene on aging and longevity

Pharmacological Modulation of Functional Phenotypes of Microglia in Neurodegenerative Diseases

Neuronal SIRT1 (Silent Information Regulator 2 Homologue 1) Regulates Glycolysis and Mediates Resveratrol-Induced Ischemic Tolerance

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