Category: Health

EGCG and inflammation

EGCG and inflammation

These data indicate that EGCG Raw sunflower seeds EGCG and inflammation from two innflammation inhibition ECGG EGCG and inflammation and improvement of insulin resistance in liver tissues. Additional inrlammation studies have collectively found that taking — mg of EGCG together with 80— mg of caffeine for at least 12 weeks is linked to significant weight loss and reduction of body fat Then, a cocktail of 80 biotinylated antibodies diluted was added at 1 ml per array membrane and membranes were kept at 4°C overnight.

Department of Inflammatiom and Metabolism, Inflxmmation of Inflamnation, Liaoning Provincial Key Laboratory of Innflammation Diseases, The First Affiliated Hospital GECG China Medical University, China Medical University.

Invlammation is anc major pharmacological compound lnflammation green tea. Nonalcoholic fatty liver disease Oxidative stress and Parkinsons disease is one of the most Interval training benefits liver diseases worldwide.

Inflammation and insulin resistance are involved in Athletes development of Herbal remedies for pain relief disease.

In EGCG and inflammation study, we investigated the beneficial effect of EGCG on oxidative stress and Parkinsons disease liver tissue inflammaiton NAFLD rats induced by a high-fat diet and its inflammtaion mechanism.

Beetroot juice for kidney health expression levels of EGCG and inflammation signaling infflammation genes EGC.

We observed that Inflammatiin decreased the triglyceride TG oxidative stress and Parkinsons disease in inflajmation livers and suppressed TLR4, TRAF6, IKKβ, ajd, p-NF-κB, and TNF-α levels compared with those in the HFD group, whereas PI3K, AKT, IRS-1, and IRS-2 indicators were improved.

EGCG improves obesity-associated subacute hepatic inflammation states, probably through the TLR4 signaling pathway. Furthermore, EGCG also alleviated hepatic insulin resistance. These data indicate that EGCG improves NAFLD from two ways: inhibition of inflammation and improvement of insulin resistance in liver tissues.

すでにアカウントをお持ちの場合 サインインは こちら. Journal of Oleo Science. Online ISSN : Print ISSN : ISSN-L : 資料トップ 早期公開 巻号一覧 この資料について. Epigallocatechin Gallate Suppresses Inflammatory Responses by Inhibiting Toll-like Receptor 4 Signaling and Alleviates Insulin Resistance in the Livers of High-fat-diet Rats.

Huimin HouWanli YangSuqing BaoYanli Cao 著者情報. Huimin Hou Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, China Medical University Wanli Yang Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, China Medical University Suqing Bao Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, China Medical University Yanli Cao Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, China Medical University.

責任著者 Corresponding author. キーワード: epigallocatechin gallateinflammationinsulin sensitivityliver tissuetoll-like receptor 4. ジャーナル フリー. PDFをダウンロード K メタデータをダウンロード RIS形式 EndNote、Reference Manager、ProCite、RefWorksとの互換性あり. graphical abstract Fullsize Image. 引用文献 関連文献 0. 電子付録 0. 前の記事 次の記事.

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: EGCG and inflammation

EGCG (Epigallocatechin Gallate): Benefits, Dosage, and Safety Yang H, Zonder JA, Dou QP: Clinical development of novel proteasome inhibitors for cancer treatment. Article CAS Google Scholar Ahmed S, Rahman A, Hasnain A, Lalonde M, Goldberg VM, Haqqi TM: Green tea polyphenol epigallocatechingallate inhibits the IL-1 beta-induced activity and expression of cyclooxygenase-2 and nitric oxide synthase-2 in human chondrocytes. Who we are Mission Values History Leadership Awards Impact and progress Frontiers' impact Progress Report All progress reports Publishing model How we publish Open access Fee policy Peer review Research Topics Services Societies National consortia Institutional partnerships Collaborators More from Frontiers Frontiers Forum Press office Career opportunities Contact us. EGCG is a type of plant compound called catechin. Asian Pac J Trop Biomed — Reilly CM, Farrelly LW, Viti D, Redmond ST, Hutchison F, Ruiz P et al. Article CAS PubMed Google Scholar Bae H-B, Li M, Kim J-P, Kim S-J, Jeong C-W, Lee H-G et al.
Introduction Fayard Optimize mobile performance, Tintignac Oxidative stress and Parkinsons disease, Baudry A, EGCCG BA. Inflammatikn of macrophage may stimulate inflammation release EGCG and inflammation inflammatory oxidative stress and Parkinsons disease also known as pro-inflammatory cytokines interleukin-β1, interleukin-6, tumor necrosis factor α [ 17 inflamation, 18 ]. ECGG novel transcript of mouse interleukin receptor acts on glomerular mesangial cells as an aggravating factor in lupus nephritis. Dingle, J. Liang YC, Chen YC, Lin YL, Lin-Shiau SY, Ho CT, Lin JK Suppression of extracellular signals and cell proliferation by the black tea polyphenol, theaflavin-3,3-digallate. Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, China Medical University. Arthritis Rheum.
Date on Master's Thesis/Doctoral Dissertation Based on the data obtained by antibody arrays, we selected IL-6, IL-8 and TNF-α expression for further confirmation as these proteins have pathophysiological relevance to OA severity and progression. Although these values are lower than those used in in vitro experiments with EGCG, an effective concentration of this catechin could be achieved by dietary supplementation. Kim J, Cha YN, Surh YJ A protective role of nuclear factor-erythroid 2-related factor-2 Nrf2 in inflammatory disorders. In comparison with steroidal or non-steroidal chemical drugs for treating inflammation, naturally derived substances for preventing prolonged inflammation have limited side effects and fewer intolerance issues, and could be available at lower costs than synthetic drugs [ 10 ]. Reilly CM, Farrelly LW, Viti D, Redmond ST, Hutchison F, Ruiz P et al. Article CAS PubMed Google Scholar Reilly CM, Farrelly LW, Viti D, Redmond ST, Hutchison F, Ruiz P et al.

EGCG and inflammation -

In this context the identification of EGCG as substance capable of affording protection or modulating the inflammatory response to CPP crystals may have important therapeutic implications. Further studies elucidating the role of EGCG dietary supplementation are needed. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

The present work was supported in part by the Italian Ministry of Education, University and Research, protocol PRINNRLXFS. Ahmed, S. Regulation of interleukin-1β-induced chemokine production and matrix metalloproteinase 2 activation by epigallocatechingallate in rheumatoid arthritis synovial fibroblasts.

Arthritis Rheum. Pubmed Abstract Pubmed Full Text CrossRef Full Text. Benito, M. Synovial tissue inflammation in early and late osteoarthritis. Busso, N. The mechanisms of inflammation in gout and pseudogout CPP-induced arthritis.

Reumatismo 63, — Dingle, J. Cartilage maintenance in osteoarthritis: interaction of cytokines, NSAID and prostaglandins in articular cartilage damage and repair. Pubmed Abstract Pubmed Full Text.

Duhon, D. The polyphenol epigallocatechingallate affects lipid rafts to block activation of the c-Met receptor in prostate cancer cells.

Fuerst, M. Calcification of articular cartilage in human osteoarthritis. Gibilisco, P. Synovial fluid crystal in osteoarthritis. Gombault, A. ATP release and purinergic signaling in NLRP3 inflammasome activation.

doi: Jaovisidha, K. Calcium crystals in osteoarthritis. Lee, M. Pharmacokinetics of tea catechins after ingestion of green tea and - -epigallocatechingallate by humans: formation of different metabolites and individual variability. Cancer Epidemiol. Biomarkers Prev.

Liu-Bryan, R. Monosodium urate and calcium pyrophosphate dihydrate crystals, inflammation, and cellular signaling. Joint Bone Spine 72, — Long, L. Artefacts in cell culture: pyruvate as a scavenger of hydrogen peroxide generated by ascorbate or epigallocatechin gallate in cell culture media.

Lotz, M. Interleukin 1 beta suppresses transforming growth factor-induced inorganic pyrophosphate PPi production and expression of the PPi-generating enzyme PC-1 in human chondrocytes.

Mak, J. Potential role of green tea catechins in various disease therapies: progress and promise. Manning, J. Analysis of catechin content of commercial green tea products. Margina, D. Quercetin and epigallocatechin gallate effects on the cell membranes biophysical properties correlate with their antioxidant potential.

Morinobu, A. Epigallocatechingallate suppresses osteoclast differentiation and ameliorates experimental arthritis in mice. Mylona, E. Enhanced interleukin-1β production of PBMCs from patients with gout after stimulation with Toll-like receptor-2 ligands and urate crystals.

Arthritis Res. Nalbant, S. Synovial fluid features and their relations to osteoarthritis severity: new findings from sequential studies.

Oliviero, F. Prevalence of calcium pyrophosphate and monosodium urate crystals in synovial fluid of patients with previously diagnosed joint diseases. Joint Bone Spine.

Olmez, U. Insulin-like growth factor-1 suppresses pyrophosphate elaboration by transforming growth factor beta1-stimulated chondrocytes and cartilage. Punzi, L. New biochemical insights into the pathogenesis of osteoarthritis and the role of laboratory investigations in clinical assessment.

Transforming growth factor-beta levels in synovial fluid of osteoarthritis with or without calcium pyrophosphate dihydrate crystals. Scanu, A. Synoviocyte cultures from synovial fluid. Reumatismo 59, 66— High-density lipoproteins downregulate CCL2 production in human fibroblast-like synoviocytes stimulated by urate crystals.

Schlesinger, N. Does acute synovitis pseudogout occur in patients with chronic pyrophosphate arthropathy pseudo-osteoarthritis? Swan, A. Evidence for a causal relationship between the structure, size, and load of calcium pyrophosphate dihydrate crystals, and attacks of pseudogout. Tsuchiya, H.

Effects of green tea catechins on membrane fluidity. Pharmacology 59, 34— Antiproliferative effects associated with membrane lipid interaction of green tea catechins. Health Sci. CrossRef Full Text. Keywords: osteoarthritis, epigallocatechingallate, inflammation, cytokines, chemokines.

Citation: Oliviero F, Sfriso P, Scanu A, Fiocco U, Spinella P and Punzi L Epigallocatechingallate reduces inflammation induced by calcium pyrophosphate crystals in vitro.

Received: 30 January ; Accepted: 01 April ; Published online: 17 April Copyright: © Oliviero, Sfriso, Scanu, Fiocco, Spinella and Punzi. This is an open-access article distributed under the terms of the Creative Commons Attribution License , which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.

e-mail: punzireu unipd. Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.

Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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Sections Sections. About journal About journal. Article types Author guidelines Editor guidelines Publishing fees Submission checklist Contact editorial office. ORIGINAL RESEARCH article Front. Epigallocatechingallate reduces inflammation induced by calcium pyrophosphate crystals in vitro.

Introduction Although osteoarthritis OA is defined as a cartilage disease, synovitis involving mononuclear cell infiltration and overexpression of proinflammatory mediators is common in early and late OA Benito et al.

Materials and Methods FLS Isolation and Treatment Synovial tissue specimens were obtained from OA patients undergoing surgical joint replacement. THP-1 Cell Culture and Treatment The human leukemic monocytic cell line THP-1, was obtained from the American Type Culture Collection Rockville, MD, USA.

Cytokine Determination The levels of interleukin IL -1β, IL-8, chemokine C—C motif ligand 2 CCL2 and transforming growth factor beta TGFβ were determined in the culture supernatants by enzyme-linked immunosorbent assay eBioscience.

MTT Assay To measure cell viability and proliferation the colorimetric MTT 3- 4,5-dimethylthiazolyl -2,5-diphenyltetrazolium bromide mitochondrial activity assay Chemicon was used. Chemotaxis Assay After inform consent, mononuclear and polymorphonuclear PMN cells were isolated from peripheral blood from healthy volunteers by density gradient centrifugation with Histopaque Sigma-Aldrich.

Statistics Results are presented as mean ± SD of n experiments performed in triplicate. Results EGCG Inhibits CPP Crystal-Induced Cytokine and Chemokine Production in FLS and THP-1 Cells In the absence of stimulus, FLS released low but significant levels of both IL-8 and CCL2 in culture supernatants Figures 1A , B.

Keywords: osteoarthritis, epigallocatechingallate, inflammation, cytokines, chemokines Citation: Oliviero F, Sfriso P, Scanu A, Fiocco U, Spinella P and Punzi L Epigallocatechingallate reduces inflammation induced by calcium pyrophosphate crystals in vitro. Edited by: Xuanwen Li , University of Pennsylvania, USA.

Antibodies used for immunoblotting were as follows: antibody against Nrf2 ab , HO-1 ab , and GAPDH ab Abcam. All the in vitro experiments were performed in triplicate and from three independent experiments unless otherwise mentioned.

The cell viability, as a preliminary study, was shown to be significantly enhanced after GTE exposure at concentrations of 2. Increase in cellular activity of keratinocyte cells 24 h after exposure.

A significant increase in keratinocyte cellular activity was detected for GTE at 2. The circle in the figure indicates the outliners.

Data is shown of 3 samples 3 wells each. Thus, LPS-treated keratinocytes showed the highest level of all pro-inflammatory cytokines and modulators tested in this study.

The protein levels of IL-β1, IL-6, and TNFα by ELISA analysis have also shown significant decrease on GTE test cell groups GTE at 2. GTE-stimulated downregulation of inflammatory markers and protein production of same markers on gingival keratinocytes exposed to LPS.

b ELISA results showed decrease in translational production of inflammatory proteins IL-1β, IL-6, and TNFα in the cells treated with GTE and LPS compared with control white bars.

Mean ± standard deviation. HEGK cells exposed to GTE at concentrations of 2. Wound closure was observed to be almost complete after 24 h in the presence of GTE 2.

Representative images are shown from 3 independent experiments and light gray areas define the areas lacking cells scale bar μm. Images were analyzed using the ImageJ software to calculate wound area. time-matched treated control for 12 h and 24 h.

In order to understand whether GTE could exert its anti-inflammatory effect through activating the Nrf2 pathway, the downstream protein HO-1 of the Nrf2 pathway was investigated in this study.

The effect of GTE on the activation of Nrf2 and the expressions of HO-1 in LPS-stimulated oral keratinocytes. The total proteins of the cells were prepared and the expressions of Nrf2 a and HO-1 b were analyzed using western blot. The purpose of this study was to ascertain the anti-inflammatory and wound healing stimulating effects of green tea extract on human gingival epithelial keratinocyte cells challenged with LPS.

Green tea also has shown antimicrobial activity against most oral bacteria. Additionally, it may enhance oral peroxidase activity and prevent the establishment and progression of periodontitis [ 27 , 28 , 29 ].

Based on its anti-inflammatory and antioxidant effects, green tea EGCG could be considered for treatment of innumerous diseases, including neurological diseases, diabetes, and hypertension [ 30 , 31 , 32 ]. Our results Fig. However, it was shown that green tea EGCG could provoke increased cytotoxicity in cells when applied at higher concentrations.

An EGCG concentration higher than μM was reported to cause production increase of H 2 O 2 and oxidative DNA damage, while concentrations of more than μM EGCG could even affect cell cycle progression [ 34 , 35 ].

Consequently, the concentration of EGCG in the test green tea solution should be carefully controlled for in in vitro assay applications. GTE solutions at 2. IL-β1 , IL-6 , and TNFα decreased in gene expression compared with those in the control, and the combination with GTE at 2.

LPS is an important component of the outer membrane of Gram-negative bacteria, which promotes cellular signal transduction through toll-like receptors and secretion of pro-inflammatory interleukins, eicosanoids, and nitric oxide [ 36 ].

As seen in cells treated only with LPS Fig. This is a predicted biological reaction to LPS bacterial endotoxin, especially from the highly oral pathogenic bacteria P.

Tumor necrosis factor α is responsible for increase in levels of inflammation by upregulating other pro-inflammatory cytokines e. Tumor necrosis factor α has been targeted by anti-inflammatory screening agents due to its multiple roles in inflammation [ 41 ].

Interleukin-β1 induces secretion of interleukin-6 and interleukin-8 which also play a role as pro-inflammatory cytokines and are important for the initiation and increase of the inflammatory response to microbial infection [ 42 ]. In addition, GTE anti-inflammatory effect was confirmed in animal studies on LPS-induced retinal inflammation [ 43 , 44 ].

Regarding the possible wound healing effect of green tea via our in vitro scratch wound healing assay, increase in difference with regard to the control was found with the GTE at concentrations of 2.

However, it has been suggested that these effects of EGCG are cancer specific and EGCG shows pronounced growth inhibitory effect on cancerous cells but not on normal cells [ 53 ].

Another study demonstrated that, in cultured skin keratinocytes, EGCG acts to enhance differentiation without triggering apoptosis [ 54 ]. Topical application of EGCG on human skin which has been identified and reported earlier results in increased cell proliferation and reduced keratinocyte apoptosis [ 55 ]; however, to the best of our knowledge, there is no report of green tea on oral cells.

Moreover, GTE at concentrations of 2. We also have to consider that any difference in green tea effects on migration likely reflects relative sensitivity of specific cell types to LPS. But further examinations of molecular basis are still needed to support this hypothesis. Regarding the signaling pathway analysis, our results showed that GTE may activate the Nrf2 pathway, bringing into play its anti-inflammatory effect on cells exposed to LPS Fig.

Also, the Nrf2-dependent anti-oxidant gene HO-1 was also increased Fig. Drugs used to activate Nrf2 pathway could be considered for use as potential oral therapies for oral inflammatory diseases, such as gingivitis or periodontitis.

Until today, there are few Nrf2 activating medicaments used in the dental clinic. Therefore, GTE could be used to develop new and safer Nrf2 activators for clinical use in dentistry.

This study has taken a step in the direction of defining the effect of green tea extract on inflammation suppression associated with wounding. However, the results are neither viewed nor are they presented as conclusive.

In addition, it is important to emphasize that problems in methodological research design of in vitro assays place limitations on interpretations. Further, the potential for green tea catechins to aid in epithelial formation bears further study.

Although this study did not support the finding of earlier animal studies [ 57 ], other research designs may yet show a benefit in its use. In addition, in vivo angiogenesis and granulation tissue augmentation by GTE have been demonstrated [ 30 ].

Therefore, further animal model research is needed. In summary, our results sustained the hypothesis that GTE attenuates the inflammation in gingival epithelial keratinocytes treated with LPS by downregulating inflammatory cytokines in a dose-dependent manner.

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Int J Morphol — Download references. We thank the Oral Microbiology Institute, Center of Dental Medicine, University of Zurich, for the donation of the human gingival epithelial keratinocyte cell line and Omnimedica AG for providing the green tea extract.

This study was further supported by Clinic of Conservative and Preventive Dentistry, Center of Dental Medicine, University of Zurich, Zurich, Switzerland. Clinic of Conservative and Preventive Dentistry, Center of Dental Medicine, University of Zurich, Zurich, Switzerland.

Disclaimer: Some links inflammaion this page are affiliate Boosting metabolism through proper nutrition that may xnd oxidative stress and Parkinsons disease a inf,ammation oxidative stress and Parkinsons disease normal pricing due to nad partnerships. This adds ZERO cost inflammmation you, and can only pass potential savings. We may receive a commission if you make a purchase through these links. See our full disclaimer here. Recently, a compound known as EGCG has emerged as a leading weight loss supplement. This new supplement offers hope for many people struggling with myriad health issues, including obesity. From pain reduction to neurological improvement, researchers are only scratching the surface when it comes to learning what it can do. Gerald Wayne Dryden, Jr. This inflammaation explores the role of lnflammation EGCGas a potential treatment for EGCG and inflammation with inflammatory bowel disease Inflwmmation. IBD is a common disorder that causes a great deal of suffering. Our understanding of the etiologies, pathogenic mechanisms, and treatment targets continues to evolve. Many new therapeutic targets are making their way through the pharmaceutical pipelines. However, not all patients benefit from these therapies. EGCG and inflammation

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