GREEN TEA (60% POLYPHENOLS, 40% CATECHINS )
Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study
Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study
Taichi Shimazu1,*, Shinichi Kuriyama1, Atsushi Hozawa1,2, Kaori Ohmori1, Yuki Sato1,3, Naoki Nakaya1, Yoshikazu Nishino4, Yoshitaka Tsubono5 and Ichiro Tsuji1
1Division of Epidemiology, Department of Public Health and Forensic Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.2Department of Health Science, Shiga University of Medical Science, Shiga, Japan.3Department of Health Policy, national Research Institute for Child Health and Development, Tokyo, Japan.4Division of pidemiology, Miyagi Cancer Center Research Institute, Natori, Japan.5Division of Health Policy, Tohoku University School of Public Policy, Sendai, Japan.
Abstract
Background Although ecological observations suggest that the Japanese diet may reduce the risk of cardiovascular disease (CVD), the impact of a Japanese dietary pattern upon mortality due to CVD is unclear.
Methods We prospectively assessed the association between dietary patterns among the Japanese and CVD mortality. Dietary information was collected from 40 547 Japanese men and women aged 40–79 years without a history of diabetes, stroke, myocardial infarction or cancer at the baseline in 1994.
Results During 7 years of follow-up, 801 participants died of CVD. Factor analysis (principal component) based on a validated food frequency questionnaire identified three dietary patterns: (i) a Japanese dietary pattern highly correlated with soybean products, fish, seaweeds, vegetables, fruits and green tea, (ii) an ‘animal food’ dietary pattern and (iii) a high-dairy, high-fruit-and-vegetable, low-alcohol (DFA) dietary pattern. The Japanese dietary pattern was related to high sodium intake and high prevalence of hypertension. After adjustment for potential confounders, the Japanese dietary pattern score was associated with a lower risk of CVD mortality (hazard ratio of the highest quartile vs the lowest, 0.73; 95% confidence interval: 0.59–0.90; P for trend = 0.003). The ‘animal food’ dietary pattern was associated with an increased risk of CVD, but the DFA dietary pattern was not.
Conclusion The Japanese dietary pattern was associated with a decreased risk of CVD mortality, despite its relation to sodium intake and hypertension.
http://ije.oxfordjournals.org/cgi/content/abstract/dym005v1
Green tea proanthocyanidins inhibit cyclooxygenase-2 expression in LPS-activated mouse macrophages: Molecular mechanisms and structure-activity relationship
Arch Biochem Biophys. 2007 Apr 1;460(1):67-74. Epub 2007 Jan 29.
Green tea proanthocyanidins inhibit cyclooxygenase-2 expression in LPS-activated mouse macrophages: Molecular mechanisms and structure-activity relationship.
Department of Biochemical Science and Technology, Faculty of Agriculture, Kagoshima University, Korimoto 1-21-24, Kagoshima City 890-0065, Japan.
The inhibitory effects of green tea proanthocyanidins on cyclooxygenase-2 (COX-2) expression and prostaglandin E(2) (PGE(2)) release were investigated in lipopolysaccharide (LPS)-activated murine macrophage RAW264 cells. Prodelphinidin B2 3,3' di-O-gallate (PDGG) caused a dose-dependent inhibition of COX-2 at both mRNA and protein levels with the attendant release of PGE(2). Molecular evidence revealed that PDGG inhibited the degradation of Ikappa-B, nuclear translocation of p65 and CCAAT/enhancer-binding protein (C/EBP)delta, and phosphorylation of c-Jun, but not CRE-binding protein (CREB), which regulate COX-2 expression. Moreover, PDGG suppressed the activations of mitogen-activated protein kinase (MAPK) including c-Jun NH(2)-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and p38 kinase. The results demonstrated that PDGG suppressed COX-2 expression via blocking MAPK-mediated activation of nuclear factor-kappaB (NF-kappaB), activator protein-1 (AP-1) and C/EBPdelta. Furthermore, studies on structure-activity relationship using five kinds of proanthocyanidins revealed that the galloyl moiety of proanthocyanidins appeared important to their inhibitory actions. Thus, our findings provide the first molecular basis that green tea proanthocyanidins with the galloyl moiety might have anti-inflammatory properties through blocking MAPK-mediated COX-2 expression.
PMID: 17313938 [PubMed - in process]
Decline in glutathione peroxidase activity is a reason for brain senescence: consumption of green tea catechin prevents the decline in its activity and protein oxidative damage in ageing mouse brain
Decline in glutathione peroxidase activity is a reason for brain senescence: consumption of green tea catechin prevents the decline in its activity and protein oxidative damage in ageing mouse brain
Takahiro Kishido1, Keiko Unno2 
, Hirotoshi Yoshida2, Daisuke Choba2, Rie Fukutomi2, Shunsuke Asahina2, Kazuaki Iguchi2, Naoto Oku1 and Minoru Hoshino2
Department of Medical Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku Shizuoka, 422-8526, Japan Laboratory of Bioorganic Chemistry, School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku Shizuoka, 422-8526, Japan
Received: 1 November 2006 Accepted: 25 January 2007 Published online: 20 February 2007
Abstract The accumulation of oxidative damage is believed to contribute to senescence. We have previously found that the consumption of green tea catechins (GT-catechin), which are potent antioxidants, decreases oxidative damage to DNA and improves brain function in aged mice with accelerated senescence (SAMP10 mice). To investigate the mechanisms underlying the beneficial effects of GT-catechin, we measured the activities of antioxidative enzymes in the brains of aged SAMP10 mice. The activity of glutathione peroxidase (GPx), an essential enzyme for reduction of hydrogen and lipid peroxides, was significantly lower in aged mice than in younger ones. However, the decline in activity was prevented in aged mice that had consumed GT-catechin. The increased level of carbonyl proteins, a marker of oxidative damage in proteins, was also significantly reduced in aged mice that had consumed GT-catechin. The activities of superoxide dismutase and catalase were not decreased in aged mice. These results suggest that decreased activity of GPx importantly contributes to brain dysfunction in ageing SAMP10 mice. Furthermore, the intake of GT-catechin protected the decline in GPx activity and age-related oxidative damage in the brain.
http://www.springerlink.com/content/26n7t878rr71n1l6/
Green Tea Polyphenols Block Endotoxin-Induced Tumor Necrosis Factor-Production and Lethality in a Murine Model
Green Tea Polyphenols Block Endotoxin-Induced Tumor Necrosis Factor-Production and Lethality in a Murine Model
Manuscript received 4 June 1998. Initial reviews completed 9 July 1998. Revision accepted 18 August 1998.
Fajun Yang*, Willem J. S. de Villiers
, Craig J. McClain
, and Gary W. Varilek**,
* Graduate Program in Nutritional Sciences, 
Department of Internal Medicine, 
Department of Internal Medicine and Graduate Programs in Toxicology and Nutritional Sciences, and ** Department of Internal Medicine, University of Kentucky and Veterans Administration Medical Center, Lexington, KY 40536
Green tea polyphenols are potent antioxidants. They have both anti-cancer and anti-inflammatory effects. However, their mechanisms of actions remain unclear. In inflammation, tumor necrosis factor-
(TNF
) plays a pivotal role. NF-KB, an oxidative stress -sensitive nuclear transcription factor, controls the expression of many genes including the TNF
gene. We postulated that green tea polyphenols regulate TNF
gene expression by modulating NF-KB activation through their antioxidant properties. In the macrophage cell line, RAW264.7, (-)epigallocatechin gallate (EGCG), the major green tea polyphenol, decreased lipopolysaccharide (LPS)-induced TNF
production in a dose-dependent fashion (50% inhibition at 100 mmol/L). EGCG also inhibited LPS-induced TNF
mRNA expression and nuclear NF-KB-binding activity in RAW264.7 cells (30-40% inhibition at 100 mmol/L). Similarly, EGCG inhibited LPS-induced TNF
production in elicited mouse peritoneal macrophages. In male BALB/c mice, green tea polyphenols (given by oral gavage 2 h prior to an i.p. injection of 40 mg LPS/kg body wt) decreased LPS-induced TNF
production in serum in a dose-responsive fashion. At a dose of 0.5 g green tea polyphenols/kg body wt, serum TNF
was reduced by 80% of control. Moreover, 0.5 g green tea polyphenols/kg body wt completely inhibited LPS-induced lethality in male BALB/c mice. We conclude that the anti-inflammatory mechanism of green tea polyphenols is mediated at least in part through down-regulation of TNF
gene expression by blocking NF-KB activation. These findings suggest that green tea polyphenols may be effective therapy for a variety of inflammatory processes.
Green Tea Extract Inhibits the Lymphatic Absorption of Cholesterol and 
-Tocopherol in Ovariectomized Rats
Green Tea Extract Inhibits the Lymphatic Absorption of Cholesterol and 
-Tocopherol in Ovariectomized Rats1 ,2
Helena B. Löest, Sang K. Noh and Sung I. Koo3
Department of Human Nutrition, Kansas State University, Manhattan, KS 66506
Evidence indicates that green tea consumption lowers the serum level of cholesterol (CH). This study was conducted to determine whether green tea lowers the intestinal absorption of CH and other lipids in ovariectomized (OX) rats. OX rats with lymph duct cannulae were infused at 3.0 mL/h for 8 h via an intraduodenal catheter with a lipid emulsion containing 14C-cholesterol (14C-CH) and 
-tocopherol (
TP) without (GT0) or with green tea extract standardized to 42.9 mg (GT1) or 120.5 mg (GT2) of total catechins in PBS (pH 6.5). Green tea extracts dose-dependently reduced (P < 0.05) the lymphatic absorption of 14C-CH. The cumulative absorptions of 14C-CH in rats infused with GT0, GT1 and GT2 were 36.3 ± 1.1, 20.7 ± 4.3 and 4.8 ± 4.1% dose, respectively. The percentage distribution of esterified CH did not differ between rats infused with GT0 and GT1 (80.2 ± 2.3% vs. 79.0 ± 1.7%), but was significantly lower in those given GT2 (69.1 ± 6.8%). The absorption of 
TP also was significantly reduced by GT1 (736.5 ± 204.9 nmol, 20.8 ± 5.8% dose) and GT2 (281.0 ± 190.8 nmol, 7.9 ± 5.4% dose) compared with GT0 (1048.8 ± 174.9 nmol, 29.6 ± 4.9% dose). The absorption of fat was significantly increased by GT1 (862.6 ± 151.1 µmol) but lowered by GT2 (557.9 ± 252.2 µmol) relative to GT0 (717.7 ± 39.1 µmol). The findings provide direct evidence that green tea has a profound inhibitory effect on the intestinal absorption of CH and 
TP in OX rats. Whether the inhibitory effect of green tea extract is attributable to a specific catechin(s) and other components in green tea remains to be determined.
Supplementation of Jurkat T Cells with Green Tea Extract Decreases Oxidative Damage Due to Iron Treatment
Supplementation of Jurkat T Cells with Green Tea Extract Decreases Oxidative Damage Due to Iron Treatment
Daniela Erba, Patrizia Riso1, Anna Colombo and Giulio Testolin
Department of Food Science and Microbiology, Division of Human Nutrition, University of Milan, Milan, Italy
Regular tea consumption has been associated with a reduced risk of cancer. As demonstrated in vitro, green tea contains catechins with antioxidant properties. We evaluated the effect of the supplementation of the Jurkat T-cell line with green tea extract on oxidative damage. Cells grown in medium with or without green tea extract (10 mg/L) were treated with Fe2+ (100 µmol/L) as an oxidative stimulus for 2 h. Cell membrane lipid peroxidation was evaluated by fatty acids pattern analysis and malondialdehyde production in 
-linolenic acid–loaded cells. Furthermore, oxidative DNA damage (single strand breaks) was detected in cells by the Comet assay and quantified as relative tail moment (RTM). Supplementation with green tea extract significantly decreased malondialdehyde production (1.6 ± 0.3 vs. 0.6 ± 0.1 nmol/mg protein, P < 0.05) and DNA damage (0.32 ± 0.07 vs. 0.12 ± 0.04 RTM, P < 0.05) after Fe2+ oxidative treatment. In control cells, there was no effect on membrane distribution of (n-3) fatty acids due to Fe2+ treatment. Cell enrichment with 
-linolenic acid increased total membrane (n-3) fatty acids. However, the oxidative treatment did not modify the distribution of polyunsaturated fatty acids. It is likely that the observed protective effects can be attributed to epigallocatechin gallate, which is present mainly (670 g/kg) in green tea extract; however, we cannot exclude contributions by other catechins. These data support a protective effect of green tea against oxidative damage.
