![Anti-inflammation action of EGCG. ROS generated by various extracellular inflammatory stimuli activate NF-B, a transcriptional factor that upregulates gene expression of proinflammation-related proteins including TNF-, IL-11, COX-2, and MMP-9 [10, 18, 73, 111, 112]. EGCG acts as an antioxidant to scavenge ROS, leading to attenuation of the effects of ROS.](https://www.researchgate.net/profile/Monira-Pervin/publication/308202926/figure/fig2/AS:631803954069505@1527645209389/Fig-3-Anti-inflammation-action-of-EGCG-ROS-generated-by-various-extracellular_Q320.jpg)
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Anti-inflammatory Action of Green Tea
Abstract and Figures
Background:
Green tea has been shown to have beneficial effects against a variety of diseases such as cancer, obesity, diabetes, cardiovascular disease, and neurodegenerative diseases. Through cellular, animal, and human experiments, green tea and its major component, epigallocatechin-3-gallate (EGCG) have been demonstrated to have anti-inflammatory effects. Our previous findings have indicated that green tea and EGCG suppress the gene and/or protein expression of inflammatory cytokines and inflammation-related enzymes.
Methods:
Using bibliographic databases, particularly PubMed (provided by the US National Library of Medicine, National Institutes of Health, United States), we examined the potential usefulness of green tea/EGCG for the prevention and treatment of inflammatory diseases in human clinical and epidemiological studies. We also reviewed results from cellular and animal experiments and proposed action mechanisms.
Results:
Most of the results from the human studies indicated the beneficial effects of green tea and tea catechins against inflammatory diseases. The cellular and animal studies also provided evidence for the favorable effects of green tea/EGCG. These results are compatible with our previous findings and can be largely explained by a mechanism wherein green tea/EGCG acts as an antioxidant to scavenge reactive oxygen species, leading to attenuation of nuclear factor-κB activity.
Conclusion:
Since green tea and EGCG have multiple targets and act in a pleiotropic manner, we may consider their usage to improve the quality of life in patients with inflammatory disease. Green tea and EGCG have beneficial health effects and no severe adverse effects; however, care should be taken to avoid overdosage, which may induce deleterious effects including hepatic injury.
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... In contrast, conjugated BAs can directly disrupt the plasma membrane and activate the protein kinase C pathway, resulting in inflammatory responses [36,37]. Such BA-induced effects may mediate metabolic and inflammation improvement by green tea consumption, as shown in previous studies [38,39]. Green tea intake has been shown to improve glucose and lipid metabolism and exhibit antiinflammatory effects [38,40]. ...
... Such BA-induced effects may mediate metabolic and inflammation improvement by green tea consumption, as shown in previous studies [38,39]. Green tea intake has been shown to improve glucose and lipid metabolism and exhibit antiinflammatory effects [38,40]. Especially, catechins, a major ingredient, can directly affect metabolic organs such as skeletal muscle and adipose tissue, and accelerate glucose uptake and lipolysis [41,42]. ...
Background/Objectives: Circulating bile acid (BA) profiles change with lifestyle and are closely related to intestinal BA metabolisms such as deconjugation and conversion to secondary BAs. The composition of BA in the blood is involved in systemic nutrient metabolism and intestinal health. Herein, we explored the associations of lifestyle and physical fitness with the circulating BA profile of middle-aged men. Methods: Data of 147 male participants (aged 50–64 years; BMI < 26 kg/m²; no medication for diabetes or dyslipidemia) from the Japan Multi-Institutional Collaborative Cohort study were analyzed. Serum concentrations of 15 types of BAs were examined for associations with variables on dietary habits, physical-activity habits, and physical fitness. Results: Green tea intake was positively associated with the deconjugation ratio of total BAs (p = 0.028) and negatively associated with secondary BA levels (free deoxycholic acid [DCA] (p = 0.078), glyco-DCA (p = 0.048), and tauro-DCA (p = 0.037)). In contrast, physical activity was negatively associated with the deconjugation ratio (p = 0.029) and secondary BA levels (free DCA (p = 0.098), and free lithocholic acid (p = 0.009)). Grip strength was also negatively associated with secondary BA levels (tauro-DCA (p = 0.041)) but was not associated with the deconjugation ratio. Energy and fat intake and skeletal muscle mass were not associated with the deconjugation ratio or secondary BA levels. Conclusions: The study findings suggest that lifestyle-associated changes in serum deconjugated and secondary BAs indicate improvements in nutrient metabolism and the intestinal environment.
... EGCG was demonstrated to exert its anti-inflammatory effects by scavenging reactive oxygen species (ROS) [43]. Previously, we have suggested ROS accumulation in tumor blood vessels in vivo [3]. ...
Background
Inflammation is one of the hallmarks of cancer and is associated with tumor growth. Tumor endothelial cells (TECs) demonstrate inflamed phenotypes. Endothelial inflammation initiates thrombus formation, which is the second cause of cancer‐related deaths. Epigallocatechin‐3‐O‐gallate (EGCG), a natural compound in green tea, has demonstrated an anti‐inflammatory effect. However, the tumor progression inhibition effect of EGCG by targeting TEC inflammation remains unclear. This study addresses the anti‐tumor effect of EGCG, especially its anti‐inflammatory role in TECs.
Methods
In vitro, the effect of EGCG on TECs were studied using real‐time quantitative PCR and immunofluoresence to analyza gene and protein expression. In vivo, a cyclic RGD liposome delivery system (MEND) was employed to efficiently deliver EGCG to TECs in tumor‐bearing mice.
Results
In vitro, EGCG significantly reduces inflammatory cytokine expression, including tumor necrosis factor‐α, interleukin‐6, IL‐8, and IL‐1β through NF‐κB signaling inhibition. Additionally, von Willebrand factor reduction in TECs, which is involved in platelet adhesion and thrombosis formation, was analyzed. Our results revealed that EGCG‐MEND significantly inhibited TEC inflammation and thrombus formation in tumors. Additionally, EGCG‐MEND improved tumor immunity by reducing programmed death‐ligand 1 expression and promoting high endothelial venule formation by recruiting CD8⁺ T cells.
Conclusion
Our results indicate the anti‐tumor potential of EGCG‐MEND in normalizing the inflammatory immune microenvironment and inhibiting thrombosis by targeting TEC.
... Multiple studies have demonstrated that flavonoids decrease NF-κB activity in inflammatory conditions [53,54]. ...
This study analyzed the phytochemical composition and functional properties of leaves and green beans from seven Arabica coffee cultivars. The total phenolic and flavonoid contents were measured using spectrophotometric methods, while caffeine, chlorogenic acid (CGA), and mangiferin levels were quantified via High-Performance Liquid Chromatography (HPLC). Volatile compounds were identified using Gas Chromatography–Mass Spectrometry (GC-MS). Antioxidant activity was assessed using 2,2-Diphenyl-1-Picrylhydrazyl (DPPH) and 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical scavenging assays, and anti-inflammatory effects were evaluated by measuring reactive oxygen species (ROS), nitric oxide (NO) levels, and nuclear factor kappa B (NF-κB) activation in lipopolysaccharide (LPS)-stimulated macrophages. The results revealed that coffee leaves had significantly higher levels of total phenols, flavonoids, and CGAs, and exhibited stronger antioxidant activities compared to green beans. Notably, Geisha leaves exhibited the highest concentrations of phenolics and flavonoids, along with potent anti-inflammatory properties. Among green beans, the Marsellesa cultivar exhibited a significant flavonoid content and strong ABTS scavenging and anti-inflammatory effects. GC-MS analysis highlighted distinct volatile compound profiles between leaves and green beans, underscoring the phytochemical diversity among cultivars. Multivariate 3D principal component analysis (PCA) demonstrated clear chemical differentiation between coffee leaves and beans across cultivars, driven by key compounds such as caffeine, CGAs, and pentadecanoic acid. Hierarchical clustering further supported these findings, with dendrograms revealing distinct grouping patterns for leaves and beans, indicating cultivar-specific chemical profiles. These results underscore the significant chemical and functional diversity across Arabica cultivars, positioning coffee leaves as a promising functional alternative to green beans due to their rich phytochemical content and bioactive properties.
... . Os benefícios farmacológicos do Aloe vera são atribuídos aos seus efeitos cicatrizantes; atividade imuno moduladora e propriedades antiinflamatórias, antioxidantes e antimicrobianas (Ali;Wahbi, 2017;Dhingra, 2014). Vários ensaios clínicos avaliaram o efeito do enxaguatório bucal com Aloe vera no biofilme e na gengivite, e os resultados apoiam o uso como um substituto eficaz da clorexidina(Chandrahas et al., 2012).Também é uma opção em creme dental considerando seu potencial antimicrobiano sobre microrganismos bucais, como Streptococos mutans e Candida albicans e melhora no índice de placa comparável àqueles que incluíam triclosan em sua composição(de Figueiredo et al., 2020;Campo Fernández et al., 2008).O chá verde, outro agente natural, possui alto teor de compostos bioativos que regulam os processos inflamatórios, e suprimem a expressão genética e proteica de citocinas inflamatórias(Ohishi et al., 2016). As propriedades anti-inflamatórias gerais do chá verde incluem a capacidade de diminuir a desnaturação de proteínas e aumentar a produção de citocinas anti-inflamatórias. ...
A periodontite é uma doença multifatorial complexa, sendo que o componente microbiano tem uma importância essencial em sua etiologia e progressão. O tratamento periodontal envolve o controle mecânico dos biofilmes supragengival e subgengival, mas nem todos os pacientes respondem de forma previsível ao tratamento. Dessa forma, o controle químico do biofilme auxilia na redução de patógenos periodontais durante o tratamento ou no retardo de recolonização bacteriana após raspagem e alisamento radicular. Vários produtos têm sido estudados para uso como terapia adjuvante e têm mostrado resultados satisfatórios. Dentre eles, os produtos naturais estão alcançando um patamar promissor. Assim, o objetivo desta revisão de literatura é avaliar o potencial antimicrobiano de extratos vegetais na microbiota bucal. Os efeitos biológicos da própolis, Aloe vera, chá verde, cranberry, calêndula, mirra e sálvia suportam o uso na cavidade bucal, com destaque a ação antimicrobiana no controle do biofilme subgengival em pacientes com periodontite. Essas substâncias também possuem atividades antiinflamatórias e antioxidantes. Apesar dos resultados encorajadores para o uso de produtos naturais na higiene bucal, novos estudos são necessários a fim de confirmarem por meio de estudos clínicos bem delineados sua aplicação clínica.
... Tea contains a variety of bioactive compounds, green tea being abundant in catechins and theanine, and black tea being abundant in theaflavins, theabrownin and caffeine, which could improve NAFLD via their anti-inflammatory, apoptosis-inducing and antioxidant abilities (5)(6)(7)(36)(37)(38) . The mechanism of the protective effect of black tea on NAFLD can be explained as follows: theabrownin, a major component of black tea, was found to inhibit obesity and NAFLD in mice through serotoninrelated signalling pathways and the gut-liver axis in animal studies (39) . ...
Tea can improve the progression of some metabolic diseases through anti-inflammatory and antioxidant effects, but its impact on non-alcoholic fatty liver disease (NAFLD) is still controversial. The aim of this paper is to identify the relationship between tea and NAFLD by Mendelian randomisation (MR) and complete clinical validation using National Health and Nutrition Examination Survey (NHANES) database. MR used data from Genome Wide Association Study, with inverse-variance weighted (IVW) as principal analytical methods. The reliability of the results was verified by a series of sensitivity and heterogeneity tests. Subsequently, clinical validation was conducted using NHANES (2005–2018), involving 22 257 participants, grouped by the type of tea. Green tea drinkers were categorised into four groups (Q1–Q4) by quartiles of green tea intake, from lowest to highest (similar for black tea drinkers and other tea drinkers). Models were constructed by logistic regression to estimate the role of tea consumption (Q1–4) on NAFLD. Finally, using fibrosis-4 index (FIB-4) to evaluate the severity of hepatic fibrosis, the effect of tea consumption (Q1–4) on the degree of hepatic fibrosis was investigated by linear regression. IVW method (OR = 0·43, 95 % CI: 0·21, 0·85, P = 0·01) and weighted median method (OR = 0·35, 95 % CI: 0·14, 0·91, P = 0·03) revealed there was a causal relationship between tea and NAFLD. An array of sensitivity analyses validated the reliability of results. Analysis of NHANES indicated tea drinker present a slightly lower prevalence of NAFLD than non-tea drinker (green tea drinkers: 47·6 %, black tea drinkers: 46·3 %, other tea drinker: 43·2 %, non-tea drinkers: 48·1 %, P < 0·05). After adjusting for confounders, compared with the lowest black tea consumption (Q1), the population with the highest black tea consumption (Q4) was independently related to lower presence of NAFLD (Q4: OR = 0·69, 95 % CI: 0·50, 0·93, P < 0·05), such association remained stable in the overweight subgroup. As further analysed, Q4 also displayed a significant negative correlation with the level of hepatic fibrosis in patients with NAFLD ( β = –0·073, 95 % CI: –0·126, −0·020, P < 0·01).Tea reduces the morbidity of NAFLD and ameliorates hepatic fibrosis degree in those already suffering from the disease.
... GTE administration effectively reduced these cytokine levels due to its antiinflammatory properties. Studies have demonstrated that green tea and its catechins (GTCs) influence the expression of inflammation-related genes and proteins, including TNF-alpha, IL-1, and MMPs [40][41][42]. ...
Background
Chronic Rapid eye movement (REM) sleep deprivation has been associated with various cardiovascular alterations, including disruptions in antioxidant defense mechanisms, lipid metabolism, and inflammatory responses. This study investigates the therapeutic potential of green tea extract (GTE) in mitigating these adverse effects.
Methods
A total of 24 male Wistar albino rats were used in this study and divided into the control group (n = 8), Chronic-REM Sleep Deprivation (CRSD) Group (n = 8) and Chronic-REM SD + Green Tea 200 (CRSD + GTE200) Group (n = 8). After 21 days, a comprehensive analysis of paraoxonase (PON1), arylesterase (ARE), malondialdehyde (MDA), glutathione (GSH), nitric oxide (NOx), proinflammatory cytokines, and lipid profiles in aortic tissue, heart tissue, and serum was conducted in a sleep-deprived rat model.
Results
Chronic REM sleep deprivation led to a significant reduction in PON1 and ARE levels in aortic (p = 0.046, p = 0.035 respectively) and heart tissues (p = 0.020, p = 0.019 respectively), indicative of compromised antioxidant defenses. MDA levels increased, and NOx levels decreased, suggesting oxidative stress and impaired vascular function. Lipid profile alterations, including increased triglycerides and total cholesterol, were observed in serum. Elevated levels of inflammatory cytokines (IL-6 and TNF-alpha) further indicated an inflammatory response (p = 0.007, p = 0.018 respectively). GTE administration demonstrated a protective role, restoring antioxidant enzyme levels, suppressing lipid peroxidation, and improving NOx levels.
Conclusion
These findings suggest the therapeutic potential of GTE in alleviating the cardiovascular impairments of chronic REM sleep deprivation, emphasizing its candidacy for further clinical exploration as a natural intervention in sleep-related disorders and associated cardiovascular risks.
Background: EGCG, the principal flavonoid found in green tea, exhibits numerous advantageous properties, notably promoting bone regeneration by enhancing the activity of osteoblasts and osteogenic differentiation. Cell-free therapy is an alternative to avoiding the side effects of cell-based therapy. By harnessing the potential of metabolites, SHED combined with EGCG can be a biomaterial to increase osteogenesis. Objectives: This study aims to assess the viability of osteoblast cells when exposed to the combination of SHED metabolites and two concentrations of EGCG, namely 10μM and 50μM. Methods: Osteoblast viability is examined with the 3-(4.5-dimethylthiazole-2-yl)2.5-diphenyl tetrazolium bromide (MTT) assays using an ELISA reader 570nm, and the absorbance value is converted to per cent form. CD50 is a parameter that indicates non-toxicity when the percentage value of living cells is more than 50%. Results: The percentage of living cells exceeded 50%, and statistically significant distinctions were observed among the control media, control cell groups, and the groups exposed to the combination of SHED metabolites and EGCG (p = 0.031). Conclusions: The viability of osteoblast cells exposed to the combination of SHED metabolites and EGCG 10µM, as well as the combination of SHED metabolites and EGCG 50µM, showed no toxicity. The combination of 10µM SHED metabolites and EGCG showed a higher osteoblast cell viability value than the combination of SHED metabolites and EGCG 50 µM.
Lipopolysaccharide- (LPS-) mediated systemic inflammation plays a critical role in neurodegenerative diseases. The present study was conducted to evaluate the protective effects of epigallocatechin gallate (EGCG), the major component in green tea, on LPS-mediated inflammation and neurotoxicity. LPS treatment of macrophages induced expression of proinflammatory cytokines (TNF-
α
, IL-1
β
, and IL-6). However, EGCG pretreatment of macrophages significantly inhibited LPS-mediated induction of these cytokines. In addition, EGCG significantly diminished LPS-induced inflammatory cytokines in the peripheral mononuclear blood cells (PBMCs). Supernatant from EGCG-pretreated and LPS-activated macrophage cultures was found to be less cytotoxic to neurons than that from non-EGCG-pretreated and LPS-activated macrophage cultures. Furthermore, EGCG treatment of neurons could inhibit LPS-induced production of reactive oxygen species (ROS). Thus EGCG represents a potent and useful neuroprotective agent for inflammation-mediated neurological disorders.
Background:
The intake of green tea has been increased recently due to its medicinal values. The antibacterial and antioxidant properties of green tea were found to be beneficial in the treatment of gingival and periodontal diseases. The aim of this comparative study was to compare the efficacy of the mouthwash containing green tea and chlorhexidine in the management of dental plaque-induced gingivitis.
Materials and methods:
Thirty patients who participated in the study were divided randomly into two groups, each group of 15 patients was prescribed with either chlorhexidine or green tea mouthwash. Turesky modification of Quigley-Hein plaque index, Löe and Silness gingival index, Ainamo and Bay bleeding index, tooth stain, and tongue stain (TS) were recorded at baseline, 15 days, and 1 month. The subjects were asked to report any discomfort or alteration in taste.
Results:
There was a significant decrease in plaque index, gingival index, and bleeding index in both the groups. However, green tea mouthwash resulted in a statistically significant decrease in bleeding index compared to chlorhexidine group. There was no significant difference in tooth stain and TS in both the groups.
Conclusion:
The green tea-containing mouthwash is equally effective in reducing the gingival inflammation and plaque to chlorhexidine.
Longevity and aging are two sides of the same coin, as they both derive from the interaction between genetic and environmental factors. Aging is a complex, dynamic biological process characterized by continuous remodeling. One of the most recent theories on aging focuses on immune response, and takes into consideration the activation of subclinical, chronic low-grade inflammation which occurs with aging, named "inflammaging". Long-lived people, especially centenarians, seem to cope with chronic subclinical inflammation through an anti-inflammatory response, called therefore "anti-inflammaging". In the present review, we have focused our attention on the contrast between inflammaging and anti-inflammaging systems, by evaluating the role of cytokines and their impact on extreme longevity. Cytokines are the expression of a network involving genes, polymorphisms and environment, and are involved both in inflammation and anti-inflammation. We have described the role of IL-1, IL-2, IL-6, IL-12, IL-15, IL-18, IL-22, IL-23, TNF-α, IFN-γ as pro-inflammatory cytokines, of IL-1Ra, IL-4, IL-10, TGF-β1 as anti-inflammatory cytokines, and of lipoxin A4 and heat shock proteins as mediators of cytokines. We believe that if inflammaging is a key to understand aging, anti-inflammaging may be one of the secrets of longevity.
. The aim of this study is to investigate whether (-)-epigallocatechin-3-gallate (EGCG) can prevent the UA-induced inflammatory effect of human umbilical vein endothelial cells (HUVEC) and the involved mechanisms in vitro.
Methods
. HUVEC were subjected to uric acid (UA) with or without EGCG treatment. RT-PCR and western blots were performed to determine the level of inflammation marker. The antioxidant activity was evaluated by measuring scavenged reactive oxygen species (ROS). Functional studies of the role of Notch-1 in HUVEC lines were performed using RNA interference analyses.
Results
. UA significantly increased the expressions of IL-6, ICAM-1, TNF-
α
, and MCP-1 and the production of ROS in HUVEC. Meanwhile, the expression of Notch-1 and its downstream effects significantly increased. Using siRNA, inhibition of Notch-1 signaling significantly impeded the expressions of inflammatory cytokines under UA treatment. Interestingly, EGCG suppressed the expressions of inflammatory cytokines and the generation of ROS. Western blot analysis of Notch-1 showed that EGCG significantly decreased the expressions of inflammatory cytokines through Notch-1 signaling pathways.
Conclusions
. In summary, our findings indicated that Notch-1 plays an important role in the UA-induced inflammatory response, and the downregulation of Notch-1 by EGCG could be an effective approach to decrease inflammation and oxidative stress induced by UA.
Tea, a product of the leaves and buds of the Camellia sinensis (Theaceae) plant, is one of the world’s most popular beverages. Tea can be broadly classified according to the production method as unfermented (green tea), half-fermented (oolong tea), fully fermented (black tea), or post-fermented (pu-erh tea). Green tea is mainly consumed in Japan and China, whereas black tea is primarily consumed in Western countries, India, and other parts of the world. The global production of green tea accounts for only 20 % of the total amount of tea produced, which is approximately one fourth of that of black tea [1]. However, green tea has been the primary target for investigations on health and nutrition among the various teas as indicated by a search conducted in the PubMed database in January 2015, which showed approximately 6020, 3340, 330, and 100 publications for the keywords “green tea,” “black tea,” “oolong tea,” and “pu-erh tea,” respectively. When combined with cancer, for example, the corresponding numbers of publications were approximately 2000, 670, 40, and 10, respectively.
Background and objective:
Over the last 10 years, bioactive plant food compounds have received considerable attention in regard to their beneficial effects against periodontal disease. In this study, we investigated the effects of black tea theaflavins (TFs) on the virulence properties of Porphyromonas gingivalis and gingival keratinocyte tight junction integrity. In addition, the effects of black tea TFs on the nuclear factor-κB (NF-κB) signaling pathway and proinflammatory cytokine/matrix metalloproteinase (MMP) secretion by monocytes/macrophages were assessed.
Material and methods:
Virulence factor gene expression in P. gingivalis was investigated by quantitative real-time PCR. A fluorescence assay was used to determine P. gingivalis adherence to, and invasion of, a gingival keratinocyte monolayer. Tight junction integrity of gingival keratinocytes was assessed by determination of transepithelial electrical resistance. Proinflammatory cytokine and MMP secretion by P. gingivalis-stimulated macrophages was quantified by ELISA. The U937-3xκB-LUC monocyte cell line transfected with a luciferase reporter gene was used to monitor NF-κB activation. Gelatin degradation was monitored using a fluorogenic assay.
Results:
Black tea TFs dose-dependently inhibited the expression of genes encoding the major virulence factors of P. gingivalis and attenuated its adherence to gingival keratinocytes. A treatment of gingival keratinocytes with black tea TFs significantly enhanced tight junction integrity and prevented P. gingivalis-mediated tight junction damage as well as bacterial invasion. Black tea TFs reduced the secretion of interleukin (IL)-1β, tumor necrosis factor-α, IL-6, chemokine (C-X-C) ligand 8, MMP-3, MMP-8 and MMP-9 by P. gingivalis-stimulated macrophages and attenuated the P. gingivalis-mediated activation of the NF-κB signaling pathway. Lastly, black tea TFs inhibited gelatin degradation by MMP-9.
Conclusion:
This study provides clear evidence that black tea TFs represent promising multifunctional therapeutic agents for prevention and treatment of periodontal disease.
Tea derived from the leaves and buds of Camellia sinensis (Theaceae) is consumed worldwide. Green tea contains various components with specific health-promoting effects, and is believed to exert protective effects against diseases including cancer, diabetes and hepatitis, as well as obesity. Of the various tea components, the polyphenol catechins have been the subject of extensive investigation and among the catechins, (-)-epigallocatechin gallate has the strongest bioactivity in most cases. Our research group has postulated that hepatocyte nuclear factor-4α, sterol regulatory element-binding proteins, and tumor necrosis factor-α are targets of green tea constituents including (-)-epigallocatechin gallate for their anti-diabetes, anti-obesity, and anti-hepatitis effects, respectively. Published papers were reviewed to determine whether the observed changes in these factors can be correlated with anti-cancer effects of green tea. Two major action mechanisms of (-)-epigallocatechin gallate have been proposed; one associated with its anti-oxidative properties and the other with its pro-oxidative activity. When reactive oxygen species are assumed to be involved, our findings that (-)-epigallocatechin gallate downregulated hepatocyte nuclear factor-4α, sterol regulatory element-binding proteins, and tumor necrosis factor-α may explain the anti-cancer effect of green tea as well. However, further studies are required to elucidate which determinant directs (-)-epigallocatechin gallate action as an anti-oxidant or a pro-oxidant for favorable activity.
The myotendinous junction (MTJ) is the weakest element in the muscle-tendon unit of the heel, and thus the most susceptible to injuries. The scarcity of adequate treatments means that tendinitis is a major concern to athletes and other groups who depend on their physical fitness, although green tea and glycine have both been shown to have beneficial effects on the inflammation. The present study investigated the remodeling effects of green tea and glycine in the MTJ of rats with tendinitis. For this, male Wistar rats were divided into five groups: animals without tendinitis and animals with tendinitis; animals with tendinitis supplied with green tea; animals with tendinitis supplied with a glycine diet; animals with tendinitis supplied with a green tea and glycine diet. Tendinitis was induced and the treatment with green tea (700mg/kg/day) and a 5% glycine diet lasted 7 days. The treatments regulated the activity of metalloproteinases (MMP)-2, 8 and -9, and induced the synthesis of type I collagen, glycosaminoglycans and non-collagenous proteins. Changes were also noted in the compaction of the collagen molecules and the amount of tenocytes. When combined, green tea and glycine modulated the inflammatory process and induced the synthesis of the elements involved in the post-lesion recovery of the tissue. The data from the MTJ were different when compared with results already published using the whole Achilles tendon. These data indicate that each region of the inflamed tendon can exhibit different responses during the treatment and therefore, modify its extracellular matrix components to facilitate recovery and repair. This article is protected by copyright. All rights reserved.
Recent studies have implicated a pathogenic role for Matrix Metalloproteinases 9 (MMP-9) in inflammatory bowel disease. Though loss of epithelial barrier function has been shown to be a key pathogenic factor for the development of intestinal inflammation, the role of MMP-9 in intestinal barrier function remains unclear. The aim of this study was to investigate the role of MMP-9 in intestinal barrier function and intestinal inflammation. Wild type (WT) and MMP-9(-/-) mice were subjected to experimental dextran sodium sulfate (DSS) colitis by administration of 3% DSS in drinking water for 7 days. The mouse colonic permeability was measured in vivo by recycling perfusion of the entire colon using fluorescent labeled dextran. The DSS-induced increase in the colonic permeability was accompanied by an increase in intestinal epithelial cell MMP-9 expression in WT mice. The DSS-induced increase in intestinal permeability and the severity of DSS colitis was found to be attenuated in MMP-9(-/-) mice. The colonic protein expression of myosin light chain kinase (MLCK), and phospho-MLC was found to be significantly increased after DSS administration in WT mice but not in MMP-9(-/-) mice. The DSS-induced increase in colonic permeability and colonic inflammation was attenuated in MLCK(-/-) mice and MLCK inhibitor ML-7 treated WT mice. DSS-induced increase in colonic surface epithelial cell MLCK mRNA was abolished in MMP-9(-/-) mice. Lastly, increased MMP-9 protein expression was detected within the colonic surface epithelial cells in ulcerative colitis cases. This data suggest role of MMP-9 in modulation of colonic epithelial permeability and inflammation via MLCK.
Cadmium (Cd), a widespread cumulative pollutant, is a known human carcinogen, associated with inflammation and tumors. Matrix metalloproteinase-9 (MMP-9) plays a pivotal role in tumor metastasis; however, the mechanisms underlying the MMP-9 expression induced by Cd remain obscure in human endothelial cells. Here, Cd elevated MMP-9 expression in dose- and time-dependent manners in human endothelial cells. Cd increased ROS production and the ROS-producing NADPH oxidase. Cd translocates p47(phox), a key subunit of NADPH oxidase, to the cell membrane. Cd also activated the phosphorylation of EGFR, Akt, Erk1/2, and JNK1/2 in addition to promoting NF-кB and AP-1 binding activities. Specific inhibitor and mutagenesis studies showed that EGFR, Akt, Erk1/2, JNK1/2 and transcription factors NF-κB and AP-1 were related to Cd-induced MMP-9 expression in endothelial cells. Akt, Erk1/2, and JNK1/2 functioned as upstream signals in the activation of NF-κB and AP-1, respectively. In addition, N-acetyl-L-cystein (NAC), diphenyleneiodonium chloride (DPI) and apocynin (APO) inhibited the Cd-induced activation of EGFR, Akt, Erk1/2, JNK1/2, and p38 MAPK, indicating that ROS production by NADPH oxidase is the furthest upstream signal in MMP-9 expression. At present, it states that Cd displayed marked invasiveness in ECV304 cells, which was partially abrogated by MMP-9 neutralizing antibodies. These results demonstrated that Cd induces MMP-9 expression via ROS-dependent EGFR->Erk1/2, JNK1/2->AP-1 and EGFR->Akt->NF-κB signaling pathways and, in turn, stimulates invasiveness in human endothelial cells.