2 Thumbs up for Green Tea

[MR. BMJ]

The Journal of Nutritional Biochemistry
Volume 18, Issue 5, May 2007, Pages 287-296

Reviews: current topics

Green tea and skin cancer: photoimmunology, angiogenesis and DNA repair

Suchitra Katiyar, Craig A. Elmets, and Santosh K. Katiyar
aDepartment of Dermatology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
bBirmingham VA Medical Center, Birmingham, AL 35294, USA
Received 15 June 2006; revised 15 July 2006; accepted 9 August 2006. Available online 17 October 2006.

Abstract Human skin is constantly exposed to numerous noxious physical, chemical and environmental agents. Some of these agents directly or indirectly adversely affect the skin. Cutaneous overexposure to environmental solar ultraviolet (UV) radiation (290–400 nm) has a variety of adverse effects on human health, including the development of melanoma and nonmelanoma skin cancers. Therefore, there is a need to develop measures or strategies, and nutritional components are increasingly being explored for this purpose. The polyphenols present in green tea (Camellia sinensis) have been shown to have numerous health benefits, including protection from UV carcinogenesis. (−)-Epigallocatechin-3-gallate (EGCG) is the major and most photoprotective polyphenolic component of green tea. In this review article, we have discussed the most recent investigations and mechanistic studies that define and support the photoprotective efficacy of green tea polyphenols (GTPs) against UV carcinogenesis. The oral administration of GTPs in drinking water or the topical application of EGCG prevents UVB-induced skin tumor development in mice, and this prevention is mediated through: (a) the induction of immunoregulatory cytokine interleukin (IL) 12; (b) IL-12-dependent DNA repair following nucleotide excision repair mechanism; (c) the inhibition of UV-induced immunosuppression through IL-12-dependent DNA repair; (d) the inhibition of angiogenic factors; and (e) the stimulation of cytotoxic T cells in a tumor microenvironment. New mechanistic information strongly supports and explains the chemopreventive activity of GTPs against photocarcinogenesis.

[MR. BMJ]

The Journal of Nutritional Biochemistry
Volume 18, Issue 9, September 2007, Pages 587-596

Research Article
Epigallocatechin-3-gallate suppresses NF-κB activation and phosphorylation of p38 MAPK and JNK in human astrocytoma U373MG cells

Abstract Epigallocatechin-3-gallate (EGCG) is the major polyphenol component of green tea and is primarily responsible for the green tea effect. EGCG possesses two triphenolic groups in its structure. These groups are reported to be important with respect to anticarcinogenic and antioxidant effects. However, the anti-inflammatory effect of EGCG on Alzheimer's disease (AD) is still not fully understood. In this study, we investigated the effects of EGCG in attenuating the inflammatory response induced by interleukin (IL)-1β+β-amyloid (25–35) fragment (Aβ) in human astrocytoma, U373MG cells. EGCG significantly inhibited the IL-1β+Aβ (25–35)-induced IL-6, IL-8, vascular endothelial growth factor (VEGF) and prostaglandin (PG)E2 production at 24 h (P<.01). The maximal inhibition rate of IL-6, IL-8, VEGF and PGE2 production by EGCG was approximately 54.40%, 56.01%, 69.06% and 47.03%, respectively. EGCG also attenuated the expression of cyclooxygenase-2 and activation of nuclear factor-κB induced by IL-1β+Aβ (25–35). We demonstrated that EGCG suppresses IL-1β+Aβ (25–35)-induced phosphorylation of the mitogen-activated protein kinase p38 and the c-Jun N-terminal kinase. In addition, EGCG induced the expression of mitogen-activated protein kinase phosphatase-1. These results provide new insight into the pharmacological actions of EGCG and its potential therapeutic application to various neurodegenerative diseases such as AD.

[MR. BMJ]

American Journal of Clinical Nutrition, Vol. 86, No. 5, 1539-1547, November 2007
ORIGINAL RESEARCH COMMUNICATION


"Chronic green tea extract supplementation reduces hemodialysis-enhanced production of hydrogen peroxide and hypochlorous acid, atherosclerotic factors, and proinflammatory cytokines1,2,3"

Shih-Ping Hsu, Ming-Shiou Wu, Chih-Ching Yang, Kuo-Chin Huang, Shaw-Yih Liou, Su-Ming Hsu and Chiang-Ting Chien

Background: Oxidative stress increases in patients with end-stage renal disease and exaggerates the related comorbidities.

Objective: The aim of the study was to evaluate the effects of supplementation with decaffeinated green tea extract (catechins) on hemodialysis-induced reactive oxygen species, atherosclerotic disease risk factors, and proinflammatory cytokines.

Design: We enrolled 6 healthy subjects and 54 hemodialysis patients for the study. First, the pharmacokinetics of one oral dose of catechins was compared between healthy subjects (n = 6) and hemodialysis patients (n = 10). Second, in the 10 hemodialysis patients, we compared the antioxidant effects of 3 different doses (0, 455, and 910 mg) of oral catechins with that of oral vitamin C (500 mg) during a hemodialysis session. Third, the other 44 hemodialysis patients participated in a 7-mo interventional study, in which 30 patients received placebo throughout and 14 patients received catechins (455 mg/d) from the third to the fifth month.

Results: After one oral dose, the hemodialysis patients (n = 10) had later peaks and slower decay of plasma catechins than did the healthy subjects. In the 10 hemodialysis patients, catechin supplementation reduced hemodialysis-enhanced plasma hypochlorous acid activity more effectively than did placebo or vitamin C. Between treatments with 455 or 910 mg catechins, no significant difference was found in the reduction of plasma hypochlorous acid activity. Catechins also significantly reduced proinflammatory cytokine expression enhanced by hemodialysis. In the 7-mo interventional study, the 14 patients who received daily supplementation of catechins for 3 mo had less predialysis plasma hydrogen peroxide activity, lower hypochlorous acid activity, and lower phosphatidylcholine hydroperoxide, C-reactive protein, and proinflammatory cytokine concentrations than did the 30 hemodialysis patients who received placebo.

Conclusion: Catechins reduce hemodialysis-induced production of hydrogen peroxide and hypochlorous acid, atherosclerotic disease risk factors, and proinflammation.

[MR. BMJ]

Journal of the American College of Nutrition, Vol. 26, No. 4, 389S-395S (2007)

"The Effects of Epigallocatechin-3-Gallate on Thermogenesis and Fat Oxidation in Obese Men: A Pilot Study"

Michael Boschmann, MD and Frank Thielecke, PhD

Objectives: The development of obesity is characterized by an increase in adipose tissue mass and by concomitant and profound changes in almost all organ functions leading to diseases such as hypertension, diabetes mellitus and coronary heart disease. Recent data from human studies indicate that the consumption of green tea and green tea extracts may help reduce body weight, mainly body fat, by increasing postprandial thermogenesis and fat oxidation. However, human studies investigating the metabolic effects of the most predominant tea catechin, EGCG, alone are absent.

Methods: In a randomized double blind, placebo-controlled, cross-over pilot study, six overweight men were given 300 mg EGCG/d for 2d. Fasting and postprandial changes in energy expenditure (EE) and substrate oxidation were assessed.

Results: Resting EE did not differ significantly between EGCG and placebo treatments, although during the first postprandial monitoring phase, respiratory quotient (RQ) values were significantly lower with EGCG compared to the placebo.

Conclusions: These findings suggest that EGCG alone has the potential to increase fat oxidation in men and may thereby contribute to the anti-obesity effects of green tea. However, more studies with a greater sample size and a broader range of age and BMI are needed to define the optimum dose.

[MR. BMJ]

Link given my Macro.

"Green Tea Polyphenol Epigallocatechin Gallate Inhibits Adipogenesis and induces apoptosis in 3T3-L1 adipocytes"

http://www.obesityresearch.org/cgi/reprint/13/6/982.pdf

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