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Organic Green Tea
Green tea contains more amount of antioxidants than any drinks or food with the same volume, and is the leaves of Camellia sinensis, undergone minimal oxidation during processing, originated from China. Green tea has been a precious drink in traditional Chinese culture and used exceptional in socialization for more than 4000 thousand years. Because of their health benefits, they have been cultivated for commercial purposes all over the world.
Sencha tea - The Ingredients of Green Sencha
Green tea contains more amount of antioxidants than any drinks or food with the same volume, and is the leaves of Camellia sinensis, undergone minimal oxidation during processing, originated from China. Green tea has been a precious drink in traditional Chinese culture and used exceptional in socialization for more than 4000 thousand years. Because of their health benefits, they have been cultivated for commercial purposes all over the world.
Sencha tea - The Ingredients of Green Sencha
Health Benefits of Green Sencha
2. Cancers
a. Cancer prevention
In the assesesment of extracts of green tea and green tea polyphenols have exhibited inhibitory effects against the formation and development of tumors at different organ sites in animals of the study of "Green tea and cancerprevention" by Yang CS, Wang X.[2a], researchers found that extracts of green tea and green tea polyphenols have suppressed cell proliferation, promoting apoptosis, and modulated signaling transduction, green teapolyphenols, especially (-)-epigallocatechin-3-gallate, also inhibit cell invasion, angiogenesis, and metastasis in skin, lung, oral cavity, esophagus, stomach, intestine, colon, liver, pancreas, bladder, mammary gland, and prostate cancers.
b. Cancer prevention
In the evaluation of green tea extracts (Camellia sinensis Theaceae) and Inhibition of tumorigenesis of the study of "Cancerprevention by tea: Evidence from laboratory studies" by Yang CS, Wang H, Li GX, Yang Z, Guan F, Jin H.[2b], researchers indicated that many studies in cell lines have demonstrated the modulation of signal transduction and metabolic pathways by (-)-epigallocatechin-3-gallate (EGCG), the most abundant and active polyphenol in green tea. These molecular events can result in cellular changes, such as enhancement of apoptosis, suppression of cell proliferation, and inhibition of angiogenesis.
c. Breast cancer
In the examination of green tea catechin and Long-term exposure to low doses of environmental carcinogens contributes to sporadic human breast cancers of the study of "Green tea catechin intervention of reactive oxygen species-mediated ERK pathway activation and chronically-induced breast cell carcinogenesis" by Rathore K, Choudhary S, Odoi A, Robert Wang HC.[2c], researchers found that GTCs (green tea catechin), at non-cytotoxic levels, were able to suppress chronically-induced cellular carcinogenesis by blocking carcinogen-induced, ROS elevation, ERK activation, cell proliferation, and DNA damage in each exposure cycle. Our model may help accelerate the identification of preventive agents to intervene in carcinogenesis induced by long-term exposure to environmental carcinogens, thereby safely and effectively reducing the health risk of sporadic breast cancer.
d. Lung cancer
in the evavuation of the importance of the antioxidant activity of green tea and EGCG for their inhibitory activity against lung tumorigenesis of the study of "The prevention of lung cancer induced by a tobacco-specific carcinogen in rodents by greenand black Tea" by Chung FL., [2d], researchers indicated that we have generated important new data that support green and black tea and caffeine as potential preventive agents against lung cancer.
e. Skin cancer
In the determination of EGCG((-)-Epigallocatechin-3-gallate) and DZNep( 3-deazaneplanocin A ) as the important candidate chemopreventive agents against skin cancer of the study of "(-)-Epigallocatechin-3-gallate and DZNep reduce polycomb protein level via a proteasome-dependent mechanism in skin cancer cells" by Choudhury SR, Balasubramanian S, Chew YC, Han B, Marquez VE, Eckert RL[2e]., researchers found that EGCG and DZNep, independently and in combination, reduce the level of PcG proteins including Ezh2, eed, Suz12, Mel18 and Bmi-1 that lead to proteasome-associated degradation.
f. Prostate cancer
In the assessment of the metabolism and bioactivity of green tea polyphenols in human prostate cancer of the study of "Green teapolyphenols and metabolites in prostatectomy tissue: implications for cancer prevention" Wang P, Aronson WJ, Huang M, Zhang Y, Lee RP, Heber D, Henning SM.[2f], researchers found that methylated and nonmethylated forms of EGCG are detectable in prostate tissue following a short-term green tea intervention, and the methylation status of EGCG may potentially modulate its preventive effect on prostate cancer.
g. Gastric, liver and esophageal cancers
In the assessment the protective effect of drinking green tea on gastric, liver and esophageal cancers of the study of "[Study on the protective effect of green tea on gastric, liver and esophageal cancers].[Article in Chinese]" by Mu LN, Zhou XF, Ding BG, Wang RH, Zhang ZF, Jiang QW, Yu SZ.[2g], researchers found that green tea decreased the development of gastric cancer risk by 40%. For individuals who drink green tea for more than 250 g per month, the risk of gastric cancer reduced about 60%. Green tea might also have protective effect on liver cancer. However, no protective effect of green tea was observed on esophageal cancer.
h. Esophageal cancer
In the assessment of inhibitory effects of greentea on the induction of esophageal cancer of the study of "Reduced risk of esophageal cancer associated with green teaconsumption" by Gao YT, McLaughlin JK, Blot WJ, Ji BT, Dai Q, Fraumeni JF Jr.[2h], researchers found that suggests a protective effect of green tea consumption. Although these findings are consistent with studies in laboratory animals, indicating that green tea can inhibit esophageal carcinogenesis, further investigations are definitely needed.
i. Stomach cancer
In the examination of the roles of green teadrinking, other risk and protective factors, and it effects on the risk of stomach cancer of the study of "Green tea drinking and multigenetic index on the risk of stomach cancer in a Chinese population" by Mu LN, Lu QY, Yu SZ, Jiang QW, Cao W, You NC, Setiawan VW, Zhou XF, Ding BG, Wang RH, Zhao J, Cai L, Rao JY, Heber D, Zhang ZF.[2i], researchers found that the protective effect of green tea drinking was observed on the risk of stomach cancer and the possible effect modification by susceptibility genes was suggested.
j. Intestinal cancer
In the evaluation of of green tea (Camellia sinensis) catechin, (-)-epigallocatechin-3-gallate (EGCG) and protective effect against intestinal cancer in the APC(min/+) mouse of the study of "Effect of genistein on the bioavailability and intestinal cancer chemopreventive activity of (-)-epigallocatechin-3-gallate" by Lambert JD, Kwon SJ, Ju J, Bose M, Lee MJ, Hong J, Hao X, Yang CS.[2j], researchers found that demonstrates that although genistein can enhance EGCG bioavailability and in vitro growth inhibitory activity, this combination enhances tumorigenesis in the APC(min/+) mouse.
k. Colon cancer
In the examination of Epigallocatechin-3-gallate (EGCG), found in green tea, and its scavenging properties of reactive oxygen species, 5-fluoruracil(5-FU) and thymoquinone(TQ) on colon cancer cells of the study of 'Comparison of potential chemotherapeutic agents, 5-fluoruracil, green tea, and thymoquinone on colon cancer cells' by Norwood AA, Tan M, May M, Tucci M, Benghuzzi H.[2k], researchers found that a similar significant decrease in cell number as early as 24 hours in the groups treated with TQ and EGCG compared to 5-FU. Increases in cellular damage were evident after 24, 48, and 72 hours and in all treated groups compared with the control.
l. cervical cancer
In the assessment of (-)-epigallocatechin-3-gallate (EGCG) in green tea and cerical cancer cell of the study of "A major constituent ofgreen tea, EGCG, inhibits the growth of a human cervical cancer cell line, CaSki cells, through apoptosis, G(1) arrest, and regulation of gene expression" by Ahn WS, Huh SW, Bae SM, Lee IP, Lee JM, Namkoong SE, Kim CK, Sin JI.[2l], reserachers found that antitumor effects of EGCG were also observed. Thus, EGCG likely provides an additional option for a new and potential drug approach for cervical cancer patients.
m. Pancreastic cancer
With an aim to evaluate the epigallocatechin gallate (EGCG) suppresses human pancreaticcancer cell proliferation of the study of 'Greentea epigallocatechin gallate exhibits anticancer effect in human pancreaticcarcinoma cells via the inhibition of both focal adhesion kinase and insulin-like growth factor-I receptor' by Vu HA, Beppu Y, Chi HT, Sasaki K, Yamamoto H, Xinh PT, Tanii T, Hara Y, Watanabe T, Sato Y, Ohdomari I.[2m], researchers suggested that blocking FAK and IGF-1R by EGCG could prove valuable for targeted therapy, which can be used in combination with other therapies, for pancreaticcancer.
n. Bladder cancer
In the examination of the antioxidant effect on bladder cancer cells of the study of "Antioxidant effects of green tea and its polyphenols on bladder cells" by Coyle CH, Philips BJ, Morrisroe SN, Chancellor MB, Yoshimura N.[2n], researchers found that urothelium cell death via H2O2-induced oxidative stress is mediated, in part, through superoxide (O2-.;), and potentially, direct H2O2 mechanisms, suggesting that green teapolyphenols can protect against oxidative stress/damage and bladder cell death.
o. Etc.
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Sources
[1] http://www.ncbi.nlm.nih.gov/pubmed/21664180
[2a] http://www.ncbi.nlm.nih.gov/pubmed/20924968
[2b] http://www.ncbi.nlm.nih.gov/pubmed/21397027
[2c] http://www.ncbi.nlm.nih.gov/pubmed/22045026
[2d] http://www.ncbi.nlm.nih.gov/pubmed/10202397
[2e] http://www.ncbi.nlm.nih.gov/pubmed/21798853
[2f] http://www.ncbi.nlm.nih.gov/pubmed/20628004
[2g] http://www.ncbi.nlm.nih.gov/pubmed/12880562
[2h] http://www.ncbi.nlm.nih.gov/pubmed/8182766
[2i] http://www.ncbi.nlm.nih.gov/pubmed/15856451
[2j] http://www.ncbi.nlm.nih.gov/pubmed/18684728
[2k] http://www.ncbi.nlm.nih.gov/pubmed/16817633
[2l] http://www.ncbi.nlm.nih.gov/pubmed/12804120
[2m] http://www.ncbi.nlm.nih.gov/pubmed/21318151
[2n] http://www.ncbi.nlm.nih.gov/pubmed/18544457
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