Green Tea - CK
Green tea is different than black teas because it is not fermented.
Polyphenols such as gallic acid and catechins such as epigallocatechin
gallate (EGCG), epigallocatechin (EGC), epicatechin gallate (ECG) and
epicatechin (EC), are abundant in green tea and are thought to be
responsible for many of its proposed benefits.
Green tea contains 2-4% caffeine or 10-80mg caffeine per cup. The
caffeine in green tea acts as a central nervous system (CNS) stimulant;
increases blood pressure, heart rate and contractility; inhibits
platelet aggregation; stimulates gastric acid secretion; and causes
Some preliminary studies show that flavonoids found in green tea might
reduce lipoprotein oxidation. In vitro tests indicate that catechins in
green tea reduce proliferation of vascular smooth muscle that occurs
with high concentrations of low-density lipoproteins (LDL). There is
some evidence that an unidentified compound in green tea and caffeine
suppresses thromboxane formation during blood clotting by inhibiting
the release of arachidonic acid from platelets.
Green tea may reduce oxidative DNA damage, lipid peroxidation and free
radical generation, and might reduce mutagenic activity in smokers.
Epigallocatechin-3-O-gallate inhibits TNFalpha-induced monocyte chemotactic protein-1 production from vascular endothelial cells
Ahn HY, Xu Y, Davidge ST.
Department of Obstetrics and Gynecology, Perinatal Research Centre,
University of Alberta, Edmonton, Canada, T6G 2S2; Department of
Physiology, Perinatal Research Centre, University of Alberta, Edmonton,
Canada, T6G 2S2; Department of Pharmacology, Chungbuk University
Gaesin-dong San 48, Cheongju, 361-763, South Korea.
Monocyte chemotactic protein-1 (MCP-1) plays a pivotal role in the
recruitment of monocytes and thus in the development of inflammatory
cardiovascular diseases. Epigallocatechin-3-O-gallate (EGCG), the major
catechin derived from green tea, has multiple beneficial effects to
reduce cardiovascular disease but the effects of EGCG on vascular
endothelial MCP-1 production is not known. In this study, we
investigated the mechanisms by which EGCG may inhibit tumor necrosis
factor-alpha (TNFalpha)-induced MCP-1 production in bovine coronary
artery endothelial cells. TNFalpha increased MCP-1 production in both a
concentration and time-dependent manner. Inhibitors of
phosphatidylinositol-3-OH kinase (PI-3 kinase), LY294002 and
wortmannin, decreased TNFalpha-induced MCP-1 production. EGCG prevented
TNFalpha-mediated MCP-1 production and reduced phosphorylation of Akt
(Ser473). In addition, EGCG attenuated TNFalpha mediated
down-regulation of TNFalpha receptor 1 (TNFR1), but not TNFR2. In
conclusion, EGCG inhibited TNFalpha-induced MCP-1 production. Moreover,
EGCG inhibited Akt phosphorylation as well as TNF activation of TNFR1,
which subsequently resulted in reduced MCP-1 production. These data
provide a novel mechanism where the green tea flavonoid, EGCG, could
provide direct vascular benefits in inflammatory cardiovascular
PMID: 18397796 [PubMed - as supplied by publisher]
The Institute of Child Health (ICH) conducted the study, published in the journal of the Federation of Experimental Biology
The team of researchers, led by Dr Anastasis Stephanou, has found that
a major chemical component of green tea (known as
epigallocatechin-3-gallate (EGCG)) can reduce cell death following a
heart attack or stroke. Cell death following these traumatic events
leads to tissue dying, and organ failure.
During a heart attack or stroke, the amount of oxygen and nutrients
reaching the brain and heart is reduced, which leads to cell death and
causes irreversible damage. Certain factors (known as STATs – Signal
Transducers and Activation of Transcription) usually become activated
in cells after a stressful event like a heart attack or stroke, causing
This particular component in green tea works against the factors that
trigger cell death, protecting the heart and brain from damage. It
also hastens the recovery of these cells. This allows the tissues to
recover, alleviating damage to the organs.
A Japanese study has suggested that green tea consumption can reduce the risk of heart disease
Researchers at the Tohoku University School of Public Policy in Sendai,
Japan, said drinking five or more 3.4-ounce cups of green tea daily
reduces the risk of heart disease by 31 percent in women and by 22
percent in men, WebMD reported Wednesday. The scientists said the
reduced risk was compared to people who consume one or fewer 3.4-ounce
cups of the beverage daily.
"Green tea may prolong your life through reducing heart disease and
stroke," said researcher Shinichi Kuriyama. "Our findings might explain
the differences in mortality profile between Japan and the United
States. The Japanese age-adjusted rate of mortality due to (heart
disease and stroke) is about 30 percent lower than that of the United
For the study, published in the Sept. 13 issue of The Journal of the
American Medical Association, researchers analyzed data collected from
40,000 healthy Japanese people aged 40 to 79 since 1994. More than 86
percent of the subjects were studied over the course of 11 years.
Protective effects of green tea polyphenol against reactive
oxygen species-induced oxidative stress in cultured rat calvarial
Park YH, Han DW, Suh H, Ryu GH, Hyon SH, Cho BK, Park JC.
Department of Medical Engineering, Cardiovascular Research Institute, Yonsei University College of Medicine Seoul, Korea.
The injurious effects of reactive oxygen species on osteoblasts and the
potential protective role played by green tea polyphenols (GtPP) were
investigated using primarily cultured rat calvarial osteoblasts.
Oxidative stress was induced in cultured osteoblasts, either by adding
100 mmol/L H2O2 or by the action of 40 U/L xanthine oxidase (XO) in the
presence of xanthine (250 micromol/L). After incubation, the cellular
viability, function and morphology were evaluated. Both treatments
produced a significant reduction in osteoblast viability, as assessed
by a two-colored fluorescence staining method combined with flow
cytometric analysis and MTT assay. A significant reduction in the
alkaline phosphatase activity was observed after H2O2 addition, whereas
XO did not have the same effect. On the microscopic observations, the
morphological changes and intracellular ultrastructural damages were
remarkably induced by both treatments. The H2O2-induced alterations
were prevented by pre-incubating the osteoblasts with 200 microg/ml
GtPP for 1 h. When the oxidative stress was induced by XO, the cellular
viability and morphology was also maintained at the same polyphenol
concentration. These results demonstrate that GtPP can act as a
biological antioxidant in a cell culture experimental model and protect
cells from oxidative stress-induced toxicity.
PMID: 14703119 [PubMed - in process]
Preservation of Human Saphenous Vein against Reactive Oxygen
Species-induced Oxidative Stress by Green Tea Polyphenol Pretreatment
Han DW, Suh H, Park YH, Cho BK, Hyon SH, Park JC.
Department of Medical Engineering and Cardiovascular Research
Institute, Yonsei University College of Medicine, Seoul, Korea; and
Institute for Frontier Medical Sciences, Kyoto University, Sakyo-ku,
The injurious effects of reactive oxygen species on venous tissues and
the potential protective role played by green tea polyphenol (GTPP) on
human saphenous veins were investigated. Oxidative stress was induced
exogenously in the vein segments, either by adding 0.8 or 1.6 M of
H2O2, or by using 80 or 160 U/L of xanthine oxidase in the presence of
xanthine (0.5 mM). After incubation, the viability of the endothelial
cells dissociated from veins and the histology of the veins were
evaluated. Due to both types of treatment, a significant decrease in
cellular viability, severe morphological changes in the veins, and
extracellular structural damage were induced. The H2O2-induced
alterations were prevented by preincubating the veins with either 0.5
or 1.0 mg/ml of GTPP for 1 h. When the oxidative stress was induced by
xanthine oxidase, cellular viability and venous structure were
preserved at the same polyphenol concentrations. These results
demonstrate that GTPP can act as a biological antioxidant and protect
veins from oxidative stress-induced toxicity.
PMID: 14678430 [PubMed - in process]