Wednesday, 29 November 2017

Food therapy: Green Tea A Potent Beverage in Reduced Risk and Treatment of Osteosarcoma

Kyle J. Norton (Scholar, Master of Nutrients, All right reserved)

Green tea may have a strong implication in reduced risk and treatment of osteosarcoma, some researchers suggested.

Green tea, a precious drink processes numbers of health benefit known to almost everyone in Asia and Western world. However, as yin in nature herbal medicine or food, long term injection of large amounts may obstruct the balance of yin-yang, induced "yin excessive syndrome" or "yang vacuity syndrome" including weaken immunity and painful case of GERD,... according to traditional Chinese medicine's Yin-Yang theory.

Osteosarcoma is a medical condition of bone cancer characterized by producing immature bone and occurred mostly in children and young adults between the ages of 10 and 30.

According to the study in investigation of the effects of Epigallocatechin-3-gallate (EGCG), in reduced risk of osteosarcoma expression in compared to miR-126 in the proliferation, invasion, migration, and chemotherapeutics resistance in cancer, application of Epigallocatechin-3-gallate (EGCG)
1. Exerted a significant effect in suppresses proliferation of human cell line osteosarcoma MG63 and U2OS cells in a concentration-dependent and time-dependent manner
2. Inhibited cancer cell line at the concentration of 0.05 g/L  on U2OS cells were equivalent to 20 μM cisplatin (DDP)

In compared to green tea extract induced cell death by interfering in cell cycle arrest, miR-126, the chemo suppressor drug induced apoptosis and inhibited proliferation in U2OS cell line but without significant effects on phase 1 of cancerous cell cycle division.

Further analysis, researchers suggested application of Epigallocatechin-3-gallate (EGCG) may increase the effect of tumor suppressing drug miR-126 and  for treatment of osteosarcoma. 

In fact, the inhibition of miR-126 osteosarcoma cells without inducing apoptosis and cells proliferation in cell cycle division is attributed to the medicine in target of sequences in reducing the expression of the targeted genes.

In other words,  the medicine can bind directly to inhibit DNA transcription and prevented  mRNA in transmitting such transcription in initiated cancer development. 

Other researchers suggested that the inhibition of Epigallocatechin-3-gallate (EGCG) in reduced cancerous cell death does not limit to the function of cell cycle arrest, the phytochemical compoud also expressed the apoptotic effect through modulating gene expression of cancer cell line and induced degradation of cancerous cellular structure.

Additional evaluation of the phytochemical Epigallocatechin-3-gallate (EGCG) and the tumor suppressed drug miR-1 effect in osteosarcoma, researchers also found that Epigallocatechin-3-gallate has a profound and positive effect in improved the efficacy of miR-1 in induced cell apoptosis and proliferation observed in cancer cell lines MG-63 and U-2OS.

More importantly, MG-63 and U-2OS treated by miR-1 and Epigallocatechin-3-gallate (EGCG) decreased c-MET expression, which is an indication of cancers development.

Further more, combined application of Epigallocatechin-3-gallate (EGCG) and c-MET inhibitor (crizotinib) also displayed a significant inhibition of MG-63 and U-2OS cancer cell proliferation.

More interestingly, in the study of the effects of Se-enriched Ziyang green tea, containing chemical compound mannose, rhamnose and fucose in anti tumor activity on human osteosarcoma U-2 OS cells in vitro and in vivo, researchers found that Se-ZYTP at concentration of 25, 50, 100 and 200 μg/ml exetred a significantly inhibition of proliferation of human osteosarcoma U-2 OS cells in a concentration-dependent fashion.

In cancer cell line In U-2 OS cancer induced in BALB/c athymic mice model, Se-ZYTP oral administration at three doses of 100, 200 and 400mg/kg body weight (B.W.) daily for 28 days resulted in tumor regression as compared to model control without causing any serious side effects.

Once again, we illustrated that other chemical compounds found in green tea may also have the  potential in suppression of  proliferation  and induced apoptosis of osteosarcoma.

In deed, the anti osteosarcoma activities of Se-enriched Ziyang green tea may be attributed to the stimulation in increased pro-apoptotic protein Bax expression(upregulated by the tumor suppressor protein p53 in induced apoptosis) and decreased  expression levels of anti-apoptotic protein Bcl-2(regulator proteins that regulate cell death) and NG2(involved cell survival, migration and angiogenesis), some researchers suggested.

Taking altogether, green tea with plenty of phytochemicals in suppression of the development and progression of cancer may be considered as an adjunct therapy in reduced risk and combination with chemo drugs for treatment of osteosarcoma.

For More information of yoga lessons tailor to a complete well being for women, please visit: YOGA BURN

Back to Kyle J. Norton Home page

Author Biography
Kyle J. Norton (Scholar, Master of Nutrients, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.

(1) Overexpression of miR-126 sensitizes osteosarcoma cells to apoptosis induced by epigallocatechin-3-gallate by Jiang L, Tao C, He A, He X1.(PubMed)
92) Green tea polyphenol EGCG suppresses osteosarcoma cell growth through upregulating miR-1 by Zhu K1, Wang W2.(PubMed)
(3) Tumoricidal effects of a selenium (Se)-polysaccharide from Ziyang green tea on human osteosarcoma U-2 OS cells by Wang Y1, Chen J, Zhang D, Zhang Y, Wen Y, Li L, Zheng L.(PubMed)

No comments:

Post a comment