Epigallocatechin‐3‐gallate (EGCG) attenuates inflammatory responses and oxidative stress in lipopolysaccharide (LPS)‐induced endometritis via silent information regulator transcript‐1 (SIRT1)/nucleotide oligomerization domain (NOD)‐like receptor pyrin domain‐containing 3 (NLRP3) pathway

Di, Man; Zhang, Qian‐Feng; Wang, Jingjing; Xiao, Xifeng; Huang, Jianlei; Ma, Yuan; Yang, Hongya; Mao, Li

doi:10.1002/jbt.23203

Cited by 8 publications

(4 citation statements)

References 45 publications

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“…An experimental study illustrated that dioscin attenuates the severity of subarachnoid hemorrhage through inhibition of NLRP3 inflammasome via a SIRT1-dependent pathway. Different studies revealed that SIRT1 has a protective effect against neurodegeneration and neuronal injury (Di et al 2022 ). SIRT1 activation by resveratrol leads to a protective effect against complications in cerebral ischemia.…”

Section: Mechanistic Role Of Sirt1 In Pdmentioning

confidence: 99%

“…SIRT1 can reduce cerebral vasospasm via modulation of the expression and activation of NLRP3 inflammasome as well as regulation of eNOS. As well, SIRT1 activation promotes ischemic tolerance by increasing HIF-1 through the SIRT1-dependent pathway (Di et al 2022 ). These findings proposed that SIRT1 activation represents a promising strategy to reduce ischemic brain injury.…”

Section: Mechanistic Role Of Sirt1 In Pdmentioning

confidence: 99%

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SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

et al. 2022

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Silent information regulator (SIRT) has distinctive enzymatic activities and physiological functions to control cell-cycle progression, gene expression, and DNA stability by targeting histone and non-histone proteins. SIRT1 enhances synaptic formation and synaptic activity, and therefore, can reduce the progression of various degenerative brain diseases including Parkinson’s disease (PD). SIRT1 activity is decreased by aging with a subsequent increased risk for the development of degenerative brain diseases. Inhibition of SIRT1 promotes inflammatory reactions since SIRT1 inhibits transcription of nuclear factor kappa B (NF-κB) which also inhibits SIRT1 activation via activation of microRNA and miR-34a which reduce NAD synthesis. SIRT1 is highly expressed in microglia as well as neurons, and has antioxidant and anti-inflammatory effects. Therefore, this review aimed to find the possible role of SIRT1 in PD neuropathology. SIRT1 has neuroprotective effects; therefore, downregulation of SIRT1 during aging promotes p53 expression and may increase the vulnerability of neuronal cell deaths. PD neuropathology is linked with the sequence of inflammatory changes and the release of pro-inflammatory cytokines due to the activation of inflammatory signaling pathways. In addition, oxidative stress, inflammatory disorders, mitochondrial dysfunction, and apoptosis contribute mutually to PD neuropathology. Thus, SIRT1 and SIRT1 activators play a crucial role in the mitigation of PD neuropathology through the amelioration of oxidative stress, inflammatory disorders, mitochondrial dysfunction, apoptosis, and inflammatory signaling pathways.

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Section: Mechanistic Role Of Sirt1 In Pdmentioning

confidence: 99%

Section: Mechanistic Role Of Sirt1 In Pdmentioning

confidence: 99%

SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

et al. 2022

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“…To date, PFDA is known to activate the NLRP3 inflammasome. In recent years, EGCG has been found to inhibit NLRP3 inflammasome-related inflammatory responses and organ damage in various animal models [49][50][51][52], and these findings revealed that EGCG is an effective natural ingredient for targeting NLRP3 inflammasome activation.…”

Section: Discussionmentioning

confidence: 95%

(−)-Epigallocatechin-3-Gallate Reduces Perfluorodecanoic Acid-Exacerbated Adiposity and Hepatic Lipid Accumulation in High-Fat Diet-Fed Male C57BL/6J Mice

Xu,

Zhong,

Wang

et al. 2023

Molecules

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Perfluorodecanoic acid (PFDA), an enduring and harmful organic pollutant, is widely employed in diverse food-related sectors. Our previous studies have provided evidence that PFDA has the potential to facilitate obesity and hepatic fat accumulation induced by high-fat diet (HFD) intake. Epigallocatechin-3-gallate (EGCG), a polyphenol found in green tea, has been suggested to possess potential preventive effects against metabolic abnormalities and fatty liver. The purpose of this research was to investigate the effects of EGCG on PFDA-exacerbated adiposity and hepatic lipid accumulation in HFD-fed mice. The results showed that EGCG reduced body weight gain; tissue and organ weights; blood glucose, serum insulin, HOMA-IR, leptin, and lipid parameters; serum inflammatory cytokines (IL−1β, IL−18, IL−6, and TNF−α); and hepatic lipid accumulation in PFDA-exposed mice fed an HFD. Further work showed that EGCG improved liver function and glucose homeostasis in mice fed an HFD and co-exposed to PFDA. The elevated hepatic mRNA levels of SREBP-1 and associated lipogenic genes, NLRP3, and caspase−1 in PFDA-exposed mice fed an HFD were significantly decreased by EGCG. Our work provides evidence for the potential anti-obesity effect of EGCG on co-exposure to HFD and PFDA and may call for further research on the bioactivity of EGCG to attenuate the endocrine disruption effects of long-term exposure to pollutants.

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“…One study showed that epigallocatechin-3gallate suppressed NLRP3 inflammasome activation. 39 Another study reported that epigallocatechin-3-gallate improved NLRP3 inflammasome activation in diabetic rats' kidneys. 40 We found docking scores of NLRP3 NACHT domain ADP and inhibitor binding sites with (-)-epicatechin as 8.8 and 8.1 respectively.…”

Section: Binding Free Energymentioning

confidence: 99%

Camellia Sinensis Çaylarındaki Moleküllerin NLRP3 NACHT Domainine İn Siliko Bağlanma Afiniteleri

DÜZGÜN,

KURAL

2023

Gümüşhane Üniversitesi Sağlık Bilimleri Dergisi

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NLRP3 inflammasome secretes proinflammatory cytokines in response to microbial infection and cellular damage, induces pyroptotic cell death, and triggers many pathological conditions. For this reason, it is important to determine the products that can inhibit the NLRP3 protein. In this study, the affinities of 27 molecules in Camellia sinensis tea species to ADP and inhibitor cavities in the NACHT domain of NLRP3 were analyzed in silico using molecular docking, molecular dynamics simulation, and free energy calculation method MM/GBSA. Among the components, theaflavic acid, (-)-epicatechin gallate and (-)-epigallocatechin gallate gave better binding affinities. It was concluded that it would be beneficial to conduct advanced studies on whether these three compounds contribute to the preventability of NLRP3-mediated inflammatory diseases.

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Epigallocatechin‐3‐gallate (EGCG) attenuates inflammatory responses and oxidative stress in lipopolysaccharide (LPS)‐induced endometritis via silent information regulator transcript‐1 (SIRT1)/nucleotide oligomerization domain (NOD)‐like receptor pyrin domain‐containing 3 (NLRP3) pathway

Cited by 8 publications

References 45 publications

SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

(−)-Epigallocatechin-3-Gallate Reduces Perfluorodecanoic Acid-Exacerbated Adiposity and Hepatic Lipid Accumulation in High-Fat Diet-Fed Male C57BL/6J Mice

Camellia Sinensis Çaylarındaki Moleküllerin NLRP3 NACHT Domainine İn Siliko Bağlanma Afiniteleri

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