EGCG has been proven to inhibit the expression of Gren Green tea extract for respiratory health lung cancer Grfen vitro 65 Boost immune system in vivo The generation of oxidative and nitrosative species, which exert their effects both directly and indirectly, is a important contributor to inflammatory injury. According to the United States Department of Agriculture USDAthe average total catechin and EGCG per mL of brewed green tea was Integr Cancer Ther. Front Nutr. Mar 1, ;91 3

Green tea extract for respiratory health -

These medications are used to treat high blood pressure and heart disease. Blood-Thinning Medications. People who take warfarin Coudamin should not drink green tea. Since green tea contains vitamin K, it can make this medication ineffective. Other compounds in green tea may slow blood clotting and therefore increase the blood-thinning effect of these medications.

You should not mix green tea and aspirin because they both prevent blood from clotting. Using the two together may increase your risk of bleeding.

If you are taking medications that promote blood thinning, discuss green tea consumption with your physician. The combination of green tea and chemotherapy medications, specifically doxorubicin and tamoxifen, increased the effectiveness of these medications in laboratory tests.

However, the same results have not been found in studies on people. On the other hand, there have been reports of both green and black tea extracts affecting a gene in prostate cancer cells that may make them less sensitive to chemotherapy drugs. For that reason, people should talk to their doctors before drinking black and green tea or taking tea extracts while undergoing chemotherapy.

Clozapine Clozaril. The effects of the clozapine may be reduced if taken within 40 minutes after drinking green tea. When taken with ephedrine, green tea may cause agitation, tremors, insomnia, and weight loss.

Green tea has been shown to reduce blood levels of lithium, a medication used to treat bipolar disorder. That can make lithium less effective. Monoamine Oxidase Inhibitors MAOIs. Green tea may cause a severe increase in blood pressure, called a "hypertensive crisis," when taken together with these drugs used to treat depression.

Examples of MAOIs include:. Birth control pills. Oral contraceptives can prolong the amount of time caffeine stays in the body, which may increase its stimulating effects. A combination of caffeine, including caffeine from green tea, and phenylpropanolamine, used in many over-the-counter and prescription cough and cold medications and weight loss products, may cause mania and a severe increase in blood pressure.

The FDA issued a public health advisory in November to warn people of the risk of bleeding in the brain from use of this medication and urged all manufacturers of this drug to remove it from the market. Most drugs that contained phenylpropanolamine have been reformulated without it.

Quinolone antibiotics. Green tea may make these medications more effective and also increase the risk of side effects. These medications include:. Other medications. Green tea, especially caffeinated green tea, may interact with a number for medications, including:.

To be safe, check with your health care provider before drinking or taking green tea if you also take other medications. Baladia E, Basulto J, Manera M, Martinez R, Calbet D. Effect of green tea or green tea extract consumption on body weight and body composition: systematic review and meta-analysis.

Nutr Hosp. Belza A, Toubro S, Astrup A. The effect of caffeine, green tea and tyrosine on thermogenesis and energy intake. Eur J Clin Nutr. Bettuzzi S, Brausi M, Rizzi F, Castagnetti G, Peracchia G, Corti A. Chemoprevention of human prostate cancer by oral administration of green tea catechins in volunteers with high-grade prostate intraepithelial neoplasia: a preliminary report from a one-year proof-of-principle study.

Cancer Res. Borrelli F, Capasso R, Russo A, Ernst E. Systematic review: green tea and gastrointestinal cancer risk. Aliment Pharmacol Ther. Mar 1, ;19 5 Boschmann M, Thielecke F. The effects of epigallocatechingallate on thermogenesis and fat oxidation in obese men: a pilot study.

J Am Coll Nutr. Brown AL, Lane J, Holyoak C, Nicol B, Mayes AE, Dadd T. Health effects of green tea catechins in overweight and obese men: a randomised controlled cross-over trial. Br J Nutr. Cooper R, Morre DJ, Morre DM.

Medicinal benefits of green tea: Part I. Review of noncancer health benefits. J Altern Complement Med. Diepvens K, Westerterp KR, Westerterp-Plantenga MS.

Obesity and thermogenesis related to the consumption of caffeine, ephedrine, capsaicin and green tea. Am J Physiol Regul Integr Comp Physiol. Fritz H, Seely D, Kennedy DA, Fernandes R, Cooley K, Fergusson D.

Green tea and lung cancer: a systemic review. Integr Cancer Ther. Fujita H, Yamagami T. Antihypercholesterolemic effect of Chinese black tea extract in human subjects with borderline hypercholesterolemia.

Nutr Res. Fukino Y, Ikeda A, Maruyama K, Aoki N, Okubo T, Iso H. Randomized controlled trial for an effect of green tea-extract powder supplementation on glucose abnormalities. Gross G, Meyer KG, Pres H, Thielert C, Tawfik H, Mescheder A. J Eur Acad Dermatol Venereol.

Hartley L, Flowers N, Holmes J, et al. Green and black tea for the primary prevention of cardiovascular disease. Cochrane Database Syst Rev. Heck AM, DeWitt BA, Lukes AL. Potential interactions between alternative therapies and warfarin. Am J Health Syst Pharm.

Hsu CH, Liao YL, Lin SC, Tsai TH, Huang CJ, Chou P. Does supplementation with green tea extract improve insulin resistance in obese type 2 diabetics? A randomized, double-blind, and placebo-controlled clinical trial. Altern Med Rev. Inoue M, Tajima K, Mizutani M, et al.

Regular consumption of green tea and the risk of breast cancer recurrence: follow-up study from the Hospital-based Epidemiologic Research Program at Aichi Cancer Center HERPACC , Japan. Cancer Lett. Jian L, Xie LP, Lee AH, Binns CW. Protective effect of green tea against prostate cancer: a case-control study in southeast China.

Int J Cancer Jan 1, ; 1 Jiao H, Hu G, Gu D, Ni X. Having a promising efficacy on type II diabetes, it's definitely a green tea time. Curr Med Chem. Jin X, Zheng RH, Li YM.

Green tea consumption and liver disease: a systematic review. Liver Int. Kato A, Minoshima Y, Yamamoto J, Adachi I, Watson AA, Nash RJ. Protective effects of dietary chamomile tea on diabetic complications. J Agric Food Chem. Khalesi S, Sun J, Buys N, et al.

Green tea catechins and blood pressure: a systematic review and meta-analysis of randomised controlled trials. Eur J Nutr. Kimura K, Ozeki M, Juneja LR, Ohira H.

L-Theanine reduces psychological and physiological stress responses. Biol Psychol. Koo SI, Noh SK. Green tea as inhibitor of the intestinal absorption of lipids: potential mechanism for its lipid-lowering effect.

J Nutr Biochem. Kovacs EM, Lejeune MP, Nijs I, Westerterp-Plantenga MS. Effects of green tea on weight maintenance after body-weight loss. Mar 1, ;91 3 Kuriyama S, Shimazu T, Ohmori K, Kikuchi N, Nakaya N, Nishino Y, Tsubono Y, Tsuji I.

Green tea consumption and mortality due to cardiovascular disease, cancer and all causes in Japan: the Ohsaki study. Lee W, Min WK, Chun S, Lee YW, Park H, Lee do H, Lee YK, Son JE.

Long-term effects of green tea ingestion on atherosclerotic biological markers in smokers. Clin Biochem. Jan 1, ;38 1 Liu K, Zhou R, Wang B, et al. Effect of green tea on glucose control and insulin sensitivity: a meta-analysis of 17 randomized controlled trials. Am J Clin Nutr.

Low Dog T, Riley D, Carter T. Traditional and alternative therapies for breast cancer. Alt Ther. Miura Y, Chiba T, Tomita I, et al. Tea catechins prevent the development of atherosclerosis in apoprotein E-deficient mice. J Nutr. Nagao T, Hase T, Tokimitsu I.

A green tea extract high in catechins reduces body fat and cardiovascular risks in humans. Obesity Silver Spring. Ho, S. Yeung, W. So, C. Cho, M. Koo, W. Lam, M. Ip, R. Man, J. Show more. Content provided by LEHVOSS Nutrition Jan White Paper.

When exploring the world of liposomal ingredients, finding the right one is key. Kaneka Ubiquinol Recorded the Nov Webinar. In partnership with Kaneka Corporation, Dr Leah Hechtman PhD will delve into the science of the antioxidant ubiquinol and its profound impact on mitochondrial Patent-pending ABB C1® redefines immune support by addressing innate, acquired, and Trained Immunity.

Our results clearly demonstrate that treatment with green tea extract exerts a protective effect and offers a novel therapeutic approach for the management of lung injury. The role of oxyradical formation in various forms of inflammation is well established [ 1 ] Reactive oxygen species ROS are associated with the inflammatory response and frequently they contribute to the tissue damaging effects of inflammatory reactions [ 2 — 4 ].

ROS formation and degradation are key components of the metabolism of aerobic organisms. Certain levels of ROS are required for normal cell functions, but if in surplus, they will cause oxidative stress [ 5 — 7 ].

ROS like superoxide, hydrogen peroxide and lipid hydroperoxides can regulate the activities of several kinases, transcription factors, cell death machinery and proteins such as COX-2 and iNOS [ 8 , 9 ].

Recent data demonstrate that the expression of the inducible isoform of nitric oxide NO synthase also plays important pathogenetic roles in various models of inflammation [ 10 — 12 ].

Peroxynitrite, a cytotoxic oxidant species formed from the reaction of NO and superoxide [ 13 ], may mediate part of the oxidative injury associated with simultaneous production of NO and oxyradicals. Peroxynitrite formation has been demonstrated in various inflammatory disorders [ 14 , 15 ] and in circulatory shock [ 16 ].

Peroxynitrite is a potent oxidant, and therefore it is conceivable that endogenous antioxidant mechanisms counteract its toxicity. In in vitro studies, it has been established that antioxidants such as glutathione, ascorbic acid, and alpha-tocopherol are scavengers of peroxynitrite and inhibitors of its oxidant capacity [ 17 , 18 ].

Green tea — a minimally processed product of the same plant that gives us black and oolong teas — is rich in powerful antioxidant compounds called polyphenols.

The polyphenols found in tea are more commonly known as flavanols or catechins and comprise 30—40 percent of the extractable solids of dried green tea leaves. The main catechins in green tea are epicatechin, epicatechingallate, epigallocatechin, and epigallocatechin gallate EGCG , with the latter being the highest in concentration.

Green tea polyphenols have demonstrated significant antioxidant, anticarcinogenic, anti-inflammatory, thermogenic, probiotic, and antimicrobial properties in numerous human, animal, and in vitro studies [ 19 , 20 ]. Recently it has been showed that green tea polyphenols inhibited tumour necrosis factor-alpha induction in macrophages by attenuating nuclear factor-kβ NF-Kβ activation [ 21 ].

Similarly [ 22 ] showed that EGCG inhibits lipopolysaccaride LPS — stimulated nitric oxide production and inducibile nitric oxide synthase gene expression in peritoneal macrophages by decreasing NF-κβ activation. These studies provide significant evidence that green tea polyphenols have anti-inflammatory effects.

Lung inflammation is characterised by T-cell rich infiltrates and enhanced expression of pro-inflammatory cytokines. The signalling pathway of IFN-γ, secreted by type-1 helper lymphocyte Th-1 , lead to the activation of signal transducer and activator of transcription-1 STAT-1 [ 23 ]. Moreover, IFN-γ is involved in the induction of iNOS and ICAM-1 gene expression by the activation of STAT-1 transcription factor [ 24 , 25 ].

Thus, upregulation of STAT-1 activity could play a key role in the pathogenesis of carrageenan-induced pleurisy. STAT-1 are activated by phosphorylation on conserved tyrosine and serine residues by the Janus kinases JAKs and MAP kinase families respectively, which allow the STAT-1 to dimerise and translocate to the nucleus and there by regulate gene expression [ 23 ].

Previously, we demonstrated, in some epithelial cell cultures, the inhibitory effect of EGCG on iNOS induction by preventing STAT-1 phosphorylation and activation [ 26 ].

In this study we investigated the role of Green tea extract in rodent model carrageenan-induced pleurisy. This experimental model has been widely used to investigate the pathophysiology of acute inflammation and also to evaluate the efficacy of drugs in inflammation.

Injection of carrageenan into the pleural space leads to pleurisy, infiltration by polymorphonuclear leukocytes PMN , and lung injury. In this study, we have investigated the effect of the green tea on: PMN infiltration [myeloperoxidase MPO activity]; STAT-1 activity by EMSA , up-regulation of ICAM-1 by immunohistochemistry ; the nitration of tyrosine residues an indicator of the formation of peroxynitrite by immunohistochemistry and lung damage histology.

Mice 4—5 weeks old, 20—22 g were purchased from Jackson Laboratories Harlan Nossan, Italy. The animals were housed in a controlled environment and provided with standard rodent chow and water.

Animal care was in compliance with Italian regulations on protection of animals used for experimental and other scientific purposes D.

Mice were anaesthetised with isoflurane and submitted to a skin incision at the level of the left sixth intercostals space. The underlying muscle was dissected and saline 0. The skin incision was closed with a suture and the animals were allowed to recover.

At 4 h after the injection of carrageenan, the animals were killed by inhalation of CO 2. The exudate and washing solution were removed by aspiration and the total volume measured. Any exudate, which was contaminated with blood, was discarded. The amount of exudate was calculated by subtracting the volume injected 1 ml from the total volume recovered.

The leukocytes in the exudate were suspended in phosphate-buffer saline PBS and counted with an optical microscope in a Burker's chamber after Blue Toluidine staining. The doses of Green Tea used here to reduce acute lung injury have been reported by us to reduce the tissue injury caused by ischemia-reperfusion in the gut dose-response curve study Muià et al submitted Myeloperoxidase MPO activity, an indicator of polymorphonuclear leukocyte PMN accumulation, was determined as previously described [ 27 ].

At 4 h after intrapleural injection of carrageenan lung tissues, were obtained and weighed. Each piece of tissue was homogenised in a solution containing 0. An aliquot of the supernatant was then allowed to react with a solution of tetra-methyl-benzidine 1. The rate of change in absorbance was measured spectrophotometrically at nm.

MPO activity was defined as the quantity of enzyme degrading 1 μmol of peroxide min at 37°C and was expressed in mill units per gram weight of wet tissue.

TNF-α levels were evaluated in the exudates at 4 h after the induction of pleurisy by carrageenan injection. The assay was carried out by using a colorimetric, commercial ELISA kit Calbiochem-Novabiochem Corporation, USA.

At the first nitrate in the supernatant was incubated with nitrate reductase 0. The nitrite concentration in the samples was measured by the Griess reaction, by adding μl of Griess reagent 0. The optical density at nm OD was measured using ELISA microplate reader SLT- Lab instruments Salzburg, Austria.

Nitrate concentrations were calculated by comparison with OD of standard solutions of sodium nitrate prepared in saline solution.

After deparaffinization, endogenous peroxidase was quenched with 0. The sections were permeabilized with 0.

Endogenous biotin or avidin binding sites were blocked by sequential incubation for 15 min with avidin and biotin. The sections were then incubated overnight with primary anti-ICAM-1 antibody , with dilution of primary antinitrotyrosine antibody DBA , and anti-PAR antibody or with control solutions.

Controls included buffer alone or non-specific purified rabbit IgG. To confirm that the immunoreaction for the nitrotyrosine was specific, some sections were also incubated with the primary antibody anti-nitrotyrosine in the presence of excess nitrotyrosine 10 mM to verify the binding specificity.

To verify the binding specificity for PARS, sections were also incubated with only the primary antibody no secondary or with only the secondary antibody no primary. In these situations, no positive staining was found in the sections, indicating that the immunoreaction was positive in all the experiments carried out.

The assay was carried out by using Optilab Graftek software on a Macintosh personal computer CPU G Lung biopsies were taken at 4 h after injection of carrageenan.

Tissue sections thickness 7 μm were deparaffinized with xylene, stained with trichromic Van Gieson, and studied using light microscopy Dialux 22 Leitz. Blood was passed on the slide, fixed at 37°C, stained with May Grunward-Giensa, and studied using light microscopy. The lung samples have been collected in liquid nitrogen and stored at °C until use.

Protein concentration in the nuclear extracts was determined using the method of [ 29 ]. The intensity of the retarded bands has been measured with a Phosphorimager Molecular Dynamic, Milan, Italy.

Unless otherwise stated, all compounds were obtained from Sigma-Aldrich Company Milan, Italy. Primary monoclonal ICAM-1 CD54 for immunoistochemistry was purchases by Pharmingen.

Reagents and secondary and nonspecific IgG antibody for immunohistochemical analysis were from Vector Laboratories InC. Primary monoclonal anti-poly ADP-ribose antibody was purchased by Alexis.

All other chemicals were of the highest commercial grade available. All stock solutions were prepared in non pyrogenic saline 0. All values in the figures and text are expressed as mean ± standard error s. of the mean of n observations.

For the in vivo studies n represents the number of animals studied. In the experiments involving histology or immunohistochemistry, the figures shown are representative of at least three experiments performed on different experimental days.

The results were analysed by one-way ANOVA followed by a Bonferroni post-hoc test for multiple comparisons. A p -value less than 0. Histological examination of lung sections revealed significant tissue damage Fig. Thus, when compared with lung sections taken from saline-treated animals Fig.

GTE significantly reduced the degree of injury as well as the infiltration of PMNs Fig. Furthermore, injection of carrageenan into the pleural cavity of mice elicited an acute inflammatory response characterized by the accumulation of fluid oedema that contained large amounts of PMNs Fig.

Oedema and PMNs infiltration in pleural cavity were attenuated by the i. injection of GTE Figs. Effect of GTE on lung injury. When compared with lung sections taken from control animals A , lung sections from carrageenan-treated mice B demonstrate interstitial haemorrhage and polymorphonuclear leukocyte accumulation B1.

Lung sections from a carrageenan-treated mice that received GTE C exhibit reduced interstitial haemorrhage and a lesser cellular infiltration. Figure is representative of all the animals in each group. Effect of GTE on carrageenan-induced inflammation. The increase in volume exudate A and accumulation of polymorphonuclear cells PMNs, B in pleural cavity 4 h after carrageenan injection was inhibited by GTE.

Data are means ± SEM of 10 mice for each group. The levels of TNF-α were significantly elevated in the exudates from vehicle-treated mice at 4 h after carrageenan administration Fig. In contrast, the levels of this pro-inflammatory cytokine was significantly lower in carrageenan-treated mice treated with GTE Fig.

No significant increased of TNF-α levels was observed in the exudates of sham-operated mice. Effect of GTE on TNF-α, level. Pleural injection of carrageenan caused by 4 h an increase in the release of the pro-inflammatory cytokines, tumour necrosis factor alpha TNF-α.

GTE significantly inhibited TNF-α. The above histological pattern of lung injury appeared to be correlated with the influx of leukocytes into the lung tissue. Therefore, we investigate the role of GTE on the neutrophils infiltration by measurement of the activity of myeloperoxidase. Effect of GTE on myeloperoxidase MPO activity in the lung.

Within 4 h, pleural injection of carrageenan led to an increase in neutrophil accumulation in the lung as measured by MPO activity GTE treatment significantly inhibited neutrophil infiltration. Staining of lung tissue sections obtained from saline-treated mice with anti-ICAM-1 antibody showed specific staining along bronchial epithelium, demonstrating that ICAM-1 is constitutively expressed data not shown.

At 4 h after carrageenan injection, the staining intensity substantially increased along the bronchial epithelium see arrows, Fig. Sections from GTE-treated mice did not reveal any up-regulation of constitutively expressed ICAM-1, which was normally expressed in the epithelium see arrows, Fig.

To verify the binding specificity for ICAM-1, some sections were also incubated with only the primary antibody no secondary. Immunohistochemical localization of ICAM-1 in the lung.

Section obtained from carrageenan-treated mice showed intense positive staining for ICAM-1 A, see arrows. The degree of bronchial epithelium see arrows staining for ICAM-1 B was markedly reduced in tissue section obtained from GTE-treated mice.

Typical Densitometry evaluation. ND: not detectable. In contrast, levels of NO x were significantly lower in the exudate of mice treated with GTE Fig.

Effect of GTE on NO production. Nitrite and nitrate concentrations in pleural exudate at 4 h after carrageenan administration.

Nitrite and nitrate levels in carrageenan-treated mice was significantly increased vs. sham group. GTE treatment significantly reduced the carrageenan-induced elevation of nitrite and nitrate levels.

At 4 h after carrageenan injection, lung sections were taken in order to determine the immunohistological staining for nitrotyrosine or PARS.

Sections of lung from saline-treated mice did not reveal any immunoreactivity for nitrotyrosine or PARS within the normal architecture data not shown.

A positive staining for nitrotyrosine Fig. GTE reduced the staining for both nitrotyrosine Fig. Therefore, no differences between groups were shown for SP-1 DNA binding activity data not shown. It was also shown the DNA binding capacity of PARP-1 to the promoter sequence of the Reg gene [ 30 ].

The retarded bands of the carraggeenan-treated mice were reduced in comparison to those of vehicle-treated or GTE pre-treated mice Fig. Immunohistochemical localization for nitrotyrosine and PARS in the lung. Immunohistochemistry for nitrotyrosine A and PARS C show positive staining along the vessels and in the bronchial epithelium from a carrageenan-treated mice.

The intensity of the positive staining for nitrotyrosine B and PARS C was significantly reduced in the lung from GTE-treated mice. Effect of GTE on PARP-1 activation.

Nuclear extracts 10 μg from lung sample were incubated with a 32 P-labeled double-stranded oligonucleotide containing binding sequence for PARP-1 and separated by nondenaturing PAGE. The specificity of the retarded bands was demonstrated by competition with fold excess of specific unlabeled oligonucleotide not shown.

B The intensity of retarded bands measured by phosphoimager in carrageenan-treated mice was significantly increased vs. GTE treatment significantly reduced the carrageenan-induced elevation of PARP-1 activity. Data are means ± SEM of 5 mice for each group. To examine the molecular mechanisms responsible for mediating the anti-inflammatory effects of GTE we measured, by EMSA, the changes in activation of the transcription factors STAT-1 and SP DNA-binding activity of STAT-1 was significantly elevated at 4 h after carrageenan administration in vehicle-treated mice Fig.

In Mice treated with green tea extract lung STAT-1 activity was similar to those of sham-operated group and significantly reduced in comparison to those of vehicle-treated mice Fig.

Effect of GTE on STAT-1 activation.

Geren is Gteen of the most popular beverages worldwide 1. Green tea extract for respiratory health is made from Green tea extract for respiratory health leaves of Camellia respirwtory. According to fro handling methods after Benefits of dietary fiber leaves are picked, tea can be categorized into 3 types: green tea, black tea, and oolong tea 2. The handling methods for green tea involve steaming or pan-frying tea leaves, while black tea involves rolling and fermenting 3. The steaming and pan-frying prevent the oxidation of polyphenols, while rolling and fermenting do not. Therefore, green tea has a much higher amount of polyphenols than does black tea 4. Catechin is the primary type of polyphenol and has numerous health-promoting properties 4.