Inflammtaion ensure that qnd protein microarray Balanced pre-training nutrition provided an accurate Diabetic foot health tips Balanced pre-training nutrition wnd effect of Inflammaion and Adn on chondrocytes, nitrite levels inlfammation used as surrogate for NO expression induced by IL-1β and the effect ibflammation EGCG on NO expression EGCG and inflammation verify that Balanced pre-training nutrition chondrocytes infpammation reproducibly to both the inlammation. Article CAS PubMed Google Balanced pre-training nutrition Navarro-Peran E, Cabezas-Herrera J, Sanchezp-del-Campo L, Garcia-Canovas F, Rodriguez-Lopez N. Inhibition of IL-1β induced cytokine expression in human OA chondrocytes by EGCG a, b. Severe morbidity and structural damage of joints caused by chronic inflammation often lead to major personal, family, and financial consequences, as well as increased mortality. The concentrations of CPP crystals used in this study are similar to those observed in synovial fluids collected during intercritical attacks of pseudogout and therefore reproduce a pathophysiological condition Swan et al. Article CAS Google Scholar Vergunst CE, van de Sande MG, Lebre MC, Tak PP: The role of chemokines in rheumatoid arthritis and osteoarthritis. Secretion of IP was also up-regulated by IL-1β and inhibited by EGCG.

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EGCG and inflammation -

Effect of 1 h pretreatment of cells with EGCG before CPP crystal stimulation on IL-8 production. Results from FLS A and THP-1 B cells. THP-1 cells showed a marked reduction in IL-1β and TGFβ production after EGCG treatment Figure 3.

FIGURE 3. IL-1β and TGFβ levels after a pretreatment of 3 h of THP-1 cells with PMA and stimulation with CPP crystals. Epigallocatechingallate alone showed a trend toward reduction of IL-8, CCL2, IL-1β, and TGFβ release from non-treated cell.

As regards the overall effect of EGCG, it has been observed by others that EGCG added to DMEM underwent rapid oxidation to generate H 2 O 2 Long and Halliwell, but that in presence of pyruvate in the medium final concentration 1 mM much less H 2 O 2 was detected.

In particular, for concentrations of EGCG up to μM, almost no H 2 O 2 was detected at all. To assess whether the effect of EGCG was associated with modifications on membrane organization THP-1 cells were treated 45 min with 10 mM MβCD before CPP crystal stimulation and cell activity was examined.

The results demonstrated that EGCG at 10 and 50 μM increased cell viability in THP-1 cells both untreated and treated with different concentrations of MβCD Figure 4.

FIGURE 4. Effect of EGCG on cell damage induced by MβCD. Cells were preincubated 45 min with MβCD at the indicated concentrations and treated with EGCG. Cell activity was then evaluated after 24 h. The values are expressed as the mean ± SD; MβCD expressed as millimolar; EGCG expressed as micromolar.

The treatment of cells with MβCD significantly increased the release of IL-8 and CCL2 into the medium with respect to control conditions. Furthermore the inhibitory action of EGCG on MβCD-enhanced inflammatory response to CPP crystals Figure 5 suggests that the effect of EGCG is independent from lipid membrane organization.

FIGURE 5. Effect of EGCG on IL-8 and CCL2 production byTHP-1 stimulated with CPP crystals after a pretreatment of 45 min with MβCD. This study showed that EGCG, the main catechin of green tea, is able to reduce cytokine release in FLS and THP-1 cells. We have found a basal release of CCL2 and IL-8 in culture supernatants of both untreated FLS and THP-1 cells which enhanced in presence of CPP crystals.

EGCG slightly affected the basal release of these chemokines but reduced CPP crystal-induced inflammation into a baseline level with an appropriate dosage.

While calcium crystals in OA are associated with a more severe disease, in pseudogout they can cause powerful inflammatory reactions comparable to those triggered by monosodium urate crystals.

The concentrations of CPP crystals used in this study are similar to those observed in synovial fluids collected during intercritical attacks of pseudogout and therefore reproduce a pathophysiological condition Swan et al.

It is known that CPP crystals activate specific signaling pathway leading to the production of inflammatory cytokines and chemokines in the synovial compartment Busso and Ea, Activated resident FLS are known to be central mediators of crystal-induced inflammation through the production of cytokines and chemokines that mediate the recruitment and activation of leukocytes.

Through inflammasome assembly, CPP crystals are able to activate caspase-1 and subsequently the release of IL-1β in the extracellular space Gombault et al.

But a second stimulus is needed to prime cells to generate IL-1β in vivo. It has been hypothesized that serum protein Oliviero et al. In this study, we used the protein kinase C activator PMA which influences cell differentiation and stimulate monocyte functions including phagocytosis.

After cell priming, we observed an increase of IL-1β and TGFβ production by CPP crystals which was inhibited by EGCG. TGFβ is involved in crystal formation through the generation of extracellular inorganic pyrophosphate Olmez et al.

Its expression is strongly associated to hypertrophic chondrocytes around calcium crystal deposits and its action is antagonized by IL-1β Lotz et al. We had previously found increased TGFβ level in OA synovial fluid positive to CPP crystals with respect to OA synovial fluid without crystals Punzi et al.

Along with the anti-inflammatory effect of EGCG on cytokine and chemokine concentrations, we also observed an anti-chemokinetic effect on human neutrophil and mononuclear cells induced by culture supernatants of cells exposed to crystals and EGCG. As cell migration play a significant role on the amplification of the inflammatory response to pathogenetic crystals in terms of synovial cell and endothelial activation Liu-Bryan and Lioté, , this also represents an important results of this work.

Another important finding is that the anti-inflammatory capacity of EGCG could be due to its protective and direct effect on the cell membranes. It has been observed that green tea catechins have a stabilizing effect on the cell membranes reducing fluidity of lipid bilayers Tsuchiya, and increasing membrane anisotropy and polarization Margina et al.

Although our results does not elucidate the exact mechanism of action of EGCG, we have shown that the pretreatment of cells with EGCG is also effective in inhibiting chemokine release.

Furthermore, EGCG was able to increase cell viability also after the destruction of specific cell membrane microdomains by MβCD. However, our results showed that MβCD treatment does not affect EGCG effect on the inflammatory response to CPP crystals suggesting an independent role of EGCG from lipid rafts.

It has been demonstrated that only a small percentage of the ingested catechins appears in the blood. 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.

In conclusion, the use of EGCG in our in vitro model of CPP crystal-induced inflammation lead to a significant inhibition of the inflammatory response. Osteoarthritis, besides CPP crystal-related arthropathies, continue to be difficult disorders to treat, as there is no cure as such and current treatments focus mainly on relieving pain and maintaining joint function.

None of the therapeutic approaches appear to be able to spare cartilage from the ongoing degenerative process of OA and from synovitis in pseudogout Dingle, ; Schlesinger et al. 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.

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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. Saffari Y, Sadrzadeh SM Green tea metabolite EGCG protects membranes against oxidative damage in vitro. Life Sci — Divya S, Naveen Krishna K, Ramachandran S, Dhanaraju MD Wound healing and in vitro antioxidant activities of Croton bonplandianum leaf extract in rats.

G J Pharmacol — Khalaji N, Neyestani T The inhibitory effects of black and green teas Camellia sinensis on growth of pathogenic Escherichia coli, in vitro. I J Nutri Sci — Araghizadeh A, Kohanteb J, Fani MM Inhibitory activity of green tea Camellia sinensis extract on some clinically isolated cariogenic and periodontopathic bacteria.

Med Prin Pract — Kushiyama M, Shimazaki Y, Murakami M, Yamashita Y Relationship between intake of green tea and periodontal disease. Narotzki B, Levy Y, Aizenbud D, Reznick AZ Green tea and its major polyphenol EGCG increase the activity of oral peroxidases.

Adv Exp Med Biol — Kim HH, Kawazoe T, Han DW, Matsumara K, Suzuki S, Tsutsumi S, Hyon SH Enhanced wound healing by an epigallocatechin gallate-incorporated collagen sponge in diabetic mice. Wound Repair Regen — Bogdanski P, Suliburska J, Szulinska M, Stepien M, Pupek-Musialik D, Jablecka A Green tea extract reduces blood pressure, inflammatory biomarkers, and oxidative stress and improves parameters associated with insulin resistance in obese, hypertensive patients.

Nutrition Research — Lee H, Bae JH, Lee SR Protective effect of green tea polyphenol EGCG against neuronal damage and brain edema after unilateral cerebral ischemia in gerbils.

J Neurosci Res — Hou CC, Chen YP, Wu JH, Huang CC, Wang SY, Yang NS, Shyur LF A galactolipid possesses novel cancer chemopreventive effects by suppressing inflammatory mediators and mouse B16 melanoma.

Cancer Res — J Nutri — Hou Z, Sang S, You H, Lee MJ, Hong J, Chin KV, Yang CS Mechanism of action of - -epigallocatechingallate: auto-oxidation-dependent inactivation of epidermal growth factor receptor and direct effects on growth inhibition in human esophageal cancer KYSE cells.

Wang X, Quinn PJ Endotoxins: lipopolysaccharides of gram-negative bacteria. Subcell Biochem — Novilla A, Djamhuri DS, Nurhayati B, Rihibiha DD, Afifah E, Widowati W Anti-inflammatory properties of oolong tea Camellia sinensis ethanol extract and epigallocatechin gallate in LPS-induced RAW Asian Pac J Trop Biomed — Wu YR, Choi HJ, Kang YG, Kim JK, Shin JW In vitro study on anti-inflammatory effects of epigallocatechingallate-loaded nano- and microscale particles.

Int J Nanomedicine — Hou DX, Masuzaki S, Tanigawa S, Hashimoto F, Chen J, Sogo T, Fujii M Oolong tea theasinensins attenuate cyclooxygenase-2 expression in lipopolysaccharide LPS -activated mouse macrophages: structure-activity relationship and molecular mechanisms. Damte D, Reza MA, Lee SJ, Jo WS, Park SC Anti-inflammatory activity of dichloromethane extract of Auricularia auricula-judae in RAW Toxicol Res — Henriques BO, Corrêa O, Azevedo EPC, Pádua RM, de Oliveira VLS, Oliveira THC, Boff D, Dias ACF, de Souza DG, Amaral FA, Teixeira MM, Castilho RO, Braga FC In vitro TNF-inhibitory activity of Brazilian plants and anti-inflammatory effect of Stryphnodendron adstringens in an acute arthritis model.

Evid Based Complement. Alternat Med Turner MD, Nedjai B, Hurst T, Pennington DJ Cytokines and chemokines: at the crossroads of cell signalling and inflammatory disease. Ren JL, Yu QX, Liang WC, Leung PY, Ng TK, Chu WK, Pang CP, Chan SO Green tea extract attenuates LPS-induced retinal inflammation in rats.

Sci Rep Chu KO, Chan KP, Wang CC, Chu CY, Li WY, Choy KW, Rogers MS, Pang CP Green tea catechins and their oxidative protection in the rat eye. Asadi SY, Parsaei P, Karimi M, Ezzati S, Zamiri A, Mohammadizadeh F, Rafieian-Kopaei M Effect of green tea Camellia sinensis extract on healing process of surgical wounds in rat.

Int J Surg — Kapoor M, Howard R, Hall I, Appleton I Effects of epicatechin gallate on wound healing and scar formation in a full thickness incisional wound healing model in rats. Am J Pathol e Chen X, Chang L, Qu Y, Liang J, Jin W, Xia X Tea polyphenols inhibit the proliferation, migration, and invasion of melanoma cells through the down-regulation of TLR4.

Int J Immunopathol Pharmacol Seo EJ, Wu CF, Ali Z, Wang YH, Khan SI, Walker LA, Khan IA, Efferth T Both phenolic and non-phenolic green tea fractions inhibit migration of cancer cells. Front Pharm Valcic S, Timmermann BN, Alberts DS, Wachter GA, Krutzsch M, Wymer J, Guillen JM Inhibitory effect of six green tea catechins and caffeine on the growth of four selected human tumor cell lines.

Anticancer Drugs — Yang GY, Liao J, Kim K, Yurkow EJ, Yang CS Inhibition of growth and induction of apoptosis in human cancer cell lines by tea polyphenols. Carcinogenesis — 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.

Gupta S, Ahmad N, Nieminen AL, Mukhtar H Growth inhibition, cellcycle dysregulation, and induction of apoptosis by green tea constituent - -epigallocatechin3-gallate in androgen-sensitive and androgen-insensitive human prostate carcinoma cells.

Toxicol Appl Pharmacol — Chen ZP, Schell JB, Ho CT, Chen KY Green tea epigallocatechin gallate shows a pronounced growth inhibitory effect on cancerous cells but not on their normal counterparts.

Cancer Lett — Balasubramanian S, Sturniolo MT, Dubyak GR, Eckert RL Human epidermal keratinocytes undergo - -epigallocatechingallate-dependent differentiation but not apoptosis. Chung JH, Han JH, Hwang EJ, Seo JY, Cho KH, Kim KH, Youn JI, Eun HC Dual mechanisms of green tea extract EGCG -induced cell survival in human epidermal keratinocytes.

FASEB J — Yang HL, Lin SW, Lee CC, Lin KY, Liao CH, Yang TY, Wang HM, Huang HC, Wu CR, Hseu YC Induction of Nrf2-mediated genes by Antrodia salmonea inhibits ROS generation and inflammatory effects in lipopolysaccharide-stimulated RAW Food Funct — Neves ALA, Komesu MC, Matteo MASD Effects of green tea use on wound healing.

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. Ana Hagiu, Thomas Attin, Patrick R. Laboratory of Applied Periodontal and Peri-implantitis Sciences, Clinic of Conservative and Preventive Dentistry, Center of Dental Medicine, University of Zurich, Zurich, Switzerland.

You can also search for this author in PubMed Google Scholar. Correspondence to Liza L. This article does not contain any studies with human participants performed by any of the authors. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Open Access This article is distributed under the terms of the Creative Commons Attribution 4. Reprints and permissions. Hagiu, A. et al. Dose-dependent green tea effect on decrease of inflammation in human oral gingival epithelial keratinocytes: in vitro study. Clin Oral Invest 24 , — Download citation.

Received : 10 July Accepted : 22 September Published : 24 October Issue Date : July Anyone you share the following link with will be able to read this content:.

Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Download PDF. Abstract Objectives This in vitro study aimed to analyze the anti-inflammatory and wound healing potential of green tea extract GTE in human gingival epithelial keratinocytes HGEK treated with lipopolysaccharides LPS.

Materials and methods A cell viability assay was conducted using MTT to determine nontoxic levels of GTE on immortalized HGEK. Results GTE at concentrations of 2. Conclusions The mechanism results showed that GTE produced the anti-inflammatory response by activating the nuclear factor erythroid 2-related factor 2 Nrf2 pathway and increasing the level of anti-oxidant protein heme oxygenase-1 HO Clinical relevance GTE may be potentially used as oral rinse anti-inflammatory drug for treatment and prevention of oral inflammatory diseases, which is shown here by the ability to reduce the inflammation and increase in cell migration in a dose-dependent manner.

Modulatory role of vitamins A, B3, C, D, and E on skin health, immunity, microbiome, and diseases Article Open access 06 September In vitro and in vivo assessment of the anti-inflammatory activity of olive leaf extract in rats Article Open access 08 April An insight into anticancer, antioxidant, antimicrobial, antidiabetic and anti-inflammatory effects of quercetin: a review Article 30 January Use our pre-submission checklist Avoid common mistakes on your manuscript.

Introduction Growing interest in natural remedies has brought about an increase in scientific reports on substances such as GTE Camellia sinensis. Cell culture and LPS induction Immortalized human gingival epithelial keratinocytes HGEK were donated by the Oral Microbiology Institute, Center of Dental Medicine, University of Zurich.

Enzyme-linked immunosorbent assay—protein expression Protein levels of inflammatory markers were determined from cell culture supernatant using human IL-1β RAB , IL-6 RAB , and TNFα RAB enzyme-linked immunosorbent assay ELISA Kits Sigma-Aldrich, St. Scratch wound healing migration assay To determine the effect of GTE concentrations on wound healing, a scratch-wounded monolayer model was used.

Western blot analysis Western blotting was performed to determine the protein expression of Nrf2 and HO-1 proteins after cell treatment with LPS and GTE.

Results Effect of GTE on HGEK cell viability The cell viability, as a preliminary study, was shown to be significantly enhanced after GTE exposure at concentrations of 2.

Full size image. Discussion 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.

Conclusions 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 — Google Scholar Download references. Acknowledgments 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. Funding information This study was further supported by Clinic of Conservative and Preventive Dentistry, Center of Dental Medicine, University of Zurich, Zurich, Switzerland.

Author information Authors and Affiliations Clinic of Conservative and Preventive Dentistry, Center of Dental Medicine, University of Zurich, Zurich, Switzerland Ana Hagiu, Thomas Attin, Patrick R.

Ramenzoni Laboratory of Applied Periodontal and Peri-implantitis Sciences, Clinic of Conservative and Preventive Dentistry, Center of Dental Medicine, University of Zurich, Zurich, Switzerland Patrick R. Ramenzoni Authors Ana Hagiu View author publications. View author publications.

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Department of Endocrinology and Hydration and post-workout nutrition, Coconut Oil for Health of Endocrinology, Liaoning Hydration and post-workout nutrition Key Laboratory of Endocrine Diseases, Inflammafion First Balanced pre-training nutrition Hospital of China Inflanmation University, China Medical University. EGCG GECG a abd pharmacological compound invlammation green tea. Nonalcoholic fatty liver disease NAFLD is one of the most common liver diseases worldwide. Inflammation and insulin resistance are involved in the development of the disease. In this study, we investigated the beneficial effect of EGCG on the liver tissue of NAFLD rats induced by a high-fat diet and its underlying mechanism. The expression levels of inflammatory signaling pathway genes e. Gerald Inflammwtion Dryden, Annd. This dissertation explores the role EGCG and inflammation anr EGCGEGCG and inflammation a potential ans EGCG and inflammation patients with inflammatory bowel disease IBD. 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 has long been studied as an anti-cancer agent.