Resveratrol pretreatment attenuates traumatic brain injury in rats by suppressing NLRP3 inflammasome activation via SIRT1

Zou, Peng; Liu, Huan; Li, Gang; Wang, Yangang

doi:10.3892/mmr.2017.8241

Cited by 72 publications

(89 citation statements)

References 34 publications

(40 reference statements)

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“…These results suggest SIRT1 might play a pivotal role of quercetin on DE in db/db mice. In addition, SIRT1 is closely related to the activation of NLRP3 inflammasome . In rat cerebral ischaemia/reperfusion models and ventilation‐induced lung injury models, SIRT1‐dependent inhibition of NLRP3 inflammatory body activation .…”

Section: Discussionmentioning

confidence: 99%

“…SIRT1 is thought to play a major role in cell proliferation, differentiation, senescence and apoptosis . Many researches have shown that SIRT1 inhibits the occurrence of inflammatory responses by negatively regulating the NLRP3 inflammasome in vascular endothelial cells . In C57BL/6 mice, quercetin rutin alleviates acute endotoxin‐induced renal injury by inhibiting inflammation and up‐regulating the expression of SIRT1 .…”

Section: Introductionmentioning

confidence: 99%

“…23,24 Many researches have shown that SIRT1 inhibits the occurrence of inflammatory responses by negatively regulating the NLRP3 inflammasome in vascular endothelial cells. 25,26 In C57BL/6 mice, quercetin rutin alleviates acute endotoxin-induced renal injury by inhibiting inflammation and up-regulating the expression of SIRT1. 27 In addition, our previous findings suggest that SIRT1 may be the key to improving cognitive function in diabetic mice.…”

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confidence: 99%

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Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

Tian

Lü

Shi

et al. 2020

J Cellular Molecular Medi

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Epidemiological studies have found that diabetes and cognitive dysfunction are closely related. Quercetin has been certified with the effect on improving diabetes mellitus (DM) and cognitive impairment. However, the effect and related mechanism of quercetin on diabetic encephalopathy (DE) are still ambiguous. In this study, we used the db/db mice (diabetic model) to discover whether quercetin could improve DE through the Sirtuin1/NLRP3 (NOD‐, LRR‐ and pyrin domain‐containing 3) pathway. Behavioural results (Morris water maze and new object recognition tests) showed that quercetin (70 mg/kg) improved the learning and memory. Furthermore, quercetin alleviated insulin resistance and the level of fasting blood glucose. Besides, Western blot analysis also showed that quercetin increased the protein expressions of nerve‐ and synapse‐related protein, including postsynapticdensity 93 (PSD93), postsynapticdensity 95 (PSD95), brain‐derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the brain of db/db mice. Quercetin also increased the protein expression of SIRT1 and decreased the expression of NLRP3 inflammation‐related proteins, including NLRP3, the adaptor protein ASC and cleaved Caspase‐1, the pro‐inflammatory cytokines IL‐1β and IL‐18. In conclusion, the present results indicate that the SIRT1/NLRP3 pathway may be a crucial mechanism for the neuroprotective effect of quercetin against DE.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

Tian

Lü

Shi

et al. 2020

J Cellular Molecular Medi

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“…Importantly, many effects of SIRT1 that are relevant to the suppression or avoidance of inflammation have been also observed upon treatment with melatonin (Figure ). In addition to the inhibition of NF‐κB activation, to Nrf2 upregulation, and to the avoidance of NLRP3 inflammasome activation, several further anti‐inflammatory actions of SIRT1 have become known. This concerns, for example, an inhibition of TLR4, which was demonstrated in renal collecting duct cells by either SIRT1 overexpression or activation by SRT1720, effects that were blocked by Sirt1 siRNA or the sirtuin inhibitors sirtinol and EX527 .…”

Section: Downstream Factors Of Melatonin's Actions With Relevance To mentioning

confidence: 99%

Melatonin and inflammation—Story of a double‐edged blade

Hardeland

2018

Journal of Pineal Research

329

350

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Melatonin is an immune modulator that displays both pro‐ and anti‐inflammatory properties. Proinflammatory actions, which are well documented by many studies in isolated cells or leukocyte‐derived cell lines, can be assumed to enhance the resistance against pathogens. However, they can be detrimental in autoimmune diseases. Anti‐inflammatory actions are of particular medicinal interest, because they are observed in high‐grade inflammation such as sepsis, ischemia/reperfusion, and brain injury, and also in low‐grade inflammation during aging and in neurodegenerative diseases. The mechanisms contributing to anti‐inflammatory effects are manifold and comprise various pathways of secondary signaling. These include numerous antioxidant effects, downregulation of inducible and inhibition of neuronal NO synthases, downregulation of cyclooxygenase‐2, inhibition of high‐mobility group box‐1 signaling and toll‐like receptor‐4 activation, prevention of inflammasome NLRP3 activation, inhibition of NF‐κB activation and upregulation of nuclear factor erythroid 2‐related factor 2 (Nrf2). These effects are also reflected by downregulation of proinflammatory and upregulation of anti‐inflammatory cytokines. Proinflammatory actions of amyloid‐β peptides are reduced by enhancing α‐secretase and inhibition of β‐ and γ‐secretases. A particular role in melatonin's actions seems to be associated with the upregulation of sirtuin‐1 (SIRT1), which shares various effects known from melatonin and additionally interferes with the signaling by the mechanistic target of rapamycin (mTOR) and Notch, and reduces the expression of the proinflammatory lncRNA‐CCL2. The conclusion on a partial mediation by SIRT1 is supported by repeatedly observed inhibitions of melatonin effects by sirtuin inhibitors or knockdown.

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“…Another study showed that resveratrol inhibited the accumulation of acetylated α-tubulin, which is a function of both cytosolic redox states and damage incurred by mitochondrial damage, thus preventing the proper assembly of the inflammasome components to elicit an inflammatory response (Misawa et al, 2015). Alternatively, the suppression of NLRP3 cytokine production and ROS by resveratrol in a separate rat TBI model was shown to be sirtuin 1 (SIRT1) dependent, illustrating the pleiotropic manner by which polyphenols suppress NLRP3 mediated neuroinflammation (Zou et al, 2018). …”

Section: Grape-derived Polyphenolic Compounds Attenuate Risk Factors mentioning

confidence: 99%

Suppression of Presymptomatic Oxidative Stress and Inflammation in Neurodegeneration by Grape-Derived Polyphenols

et al. 2018

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Neurodegenerative disorders constitute a group of multifaceted conditions characterized by the progressive loss of neurons and synaptic connections consequent to a combination of specific genetic predispositions and stochastic stressors. The neuropathologies observed in both Alzheimer’s and Parkinson’s disease are in part attributed to compounding intrinsic and extrinsic environmental stressors, which we propose may be limited by the administration of specific grape derived phytochemicals and their metabolized derivatives, specifically polyphenols isolated from grape botanicals. Current therapies for neurodegenerative disorders are limited as they solely target the final disease pathologies including behavioral changes, cognitive deficits, proteinopathies and neuronal loss; however, this strategy is not a sustainable approach toward managing disease onset or progression. This review discusses the application of grape derived polyphenols as an adjunctive treatment paradigm for the prevention of neuropathologies associated with Alzheimer’s disease, Parkinson’s disease and Chronic Traumatic Encephalopathy by simultaneously ameliorating two stochastic stressors that facilitate their disease pathologies: inflammation and oxidative stress. The biophysical attributes of grape-derived polyphenols buffer against redox potential dependent peripheral and neuroinflammation and down regulate the activation of inflammasomes in microglia and astrocytes, which could provide a novel mechanism through which grape-derived polyphenols simultaneously suppress risk factors across pathologically distinct neurodegenerative conditions. This approach therefore offers a prophylactic mode, not feasible through current pharmacological agents, to target activity dependent risk factors for neurodegenerative disorders that manifest over an individual’s lifetime.

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Resveratrol pretreatment attenuates traumatic brain injury in rats by suppressing NLRP3 inflammasome activation via SIRT1

Cited by 72 publications

References 34 publications

Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

Melatonin and inflammation—Story of a double‐edged blade

Suppression of Presymptomatic Oxidative Stress and Inflammation in Neurodegeneration by Grape-Derived Polyphenols

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