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Herbal Therapy: Green Tea, a Functional Food in Attenuated

Risk and Treatment of Autoimmune Diseases

Kyle J. Norton (All right reserved)

Green tea bioactive Epigallocatechin-3-gallate (EGCG) may have a therapeutic


and profound effect in attenuated risk and treatment of autoimmune diseases,
some scientists postulated.

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.

Autoimmune diseases are class of diseases characterized by immune system in


attacking its own tissues.

Green tea bioactive compound Epigallocatechin-3-gallate (EGCG) in risk of


autoimmune diseases was found to associate to many different mechanisms
involved numbers of aspect.

In interleukin-1 receptor antagonist knockout (IL-1raKO) arthritis rodent


models of human rheumatoid arthritis, intraperitoneal injection of EGCG three
times per week after the first immunization showed a significant reduction of
arthritis index observed by decreased damage and destruction of joint tissues.

The efficacy of green tea phytochemicals in inhibited arthritis expression was


attributed to the activities in reduced production of pro-inflammatory cytokines
in accumulation of inflammatory cells into the synovium for joint destruction
and oxidative stress proteins in facilitated inflammation and destruction of the
joints in arthritis.

Furthermore, the extract also exhibited anti STAT3 expression in mediated


variety of genes in response to cell stimuli to induce cellular processes such as
cell growth and division, cell movement, and apoptosis activated by cytokine-
dependent inflammation, through phosphorylation-Stat3 Antibody (y705) and
(S727)in shortening the duration of STAT3 activity.
Interestingly, additional analysis also found that application of green tea
bioactive compound lowers the mediation effect of mammalian target of
rapamycin (mTOR) function in limited production of pro inflammatory
cytokines and hypoxia-inducible factor 1 (HIF-1) in regulation of vascular
endothelial growth factor (VEGF) function in activated pro inflammatory
expression in innate immunity.

Moreover, injection of EGCG also exhibited anti-osteoclastic activity observed


by reduced osteoclast markers in EGCG-treated IL-1RaKO mice.

In mice induced Sjögren's syndrome with pathogenic effects of reactive oxygen


species (ROS) in the salivary glands, administration of green tea
Epigallocatechin gallate (EGCG), was found to reduce over expression of ROS
in precipitated oxidative stress-induced DNA damage and apoptosis in MRL-
Fas(lpr) mice with autoimmune sialadenitis through Heme oxygenase(HO)-1 in
response to pro antioxidant expression and Bcl-2 with function to induce cell
survival.

Additionally, in the investigation of the ameliorated effects of green tea in risk


of autoimmune sialadenitis in a murine model, application of the green tea
extract chemical compound decreased severity of sialadenitis substantially
through reduced expressions of Thymine glycol (5,6-dihydroxy-5,6-
dihydrothymine) with function in induced DNA damage.by oxidation and
ionizing radiation andgp91phox subunit of NADPH oxidase in production of
ROS to react to the acute phase of infection.

Further differentiation indicated that the chemical constituents also ameliorated


single-stranded DNA (ssDNA) function in DNA duplication in both viruses and
organisms and cleaved caspase 3 activity in mediation of programmed cell
death and TP53 or tumor protein in regulated apoptosis mediated by expression
of BAX.

More profoundly, in the examine duct epithelial cells of salivary glands,


EGCG-treated mice showed decreased levels of SS-A/Ro, an extractable
nuclear antigen (ENA) and Sjögren syndrome antigen B or Lupus La protein
(SSB/La) associated with auto immune diseases such as systemic lupus
erythematosus (SLE) and Sjögren's syndrome (SS).

Finally, green tea EGCG-treated mice also showed a lower Ifi202b interferon
activated gene 202B expression in implicated the development of systemic
lupus erythematosus (SLE) and Ifi202 over expression in the kidney and
immune organs, an indication of significantly increased disease progression in
autoimmune glomerulonephritis, according to publication of Gene ID: 26388,
updated on 5-Nov-2017.

Taken together, green tea processed abundantly bioactive phytochemicals may


be considered as a functional food in reduced risk and treatment of auto
immune diseases. Intake of green tea extract should be taken with care as
overdose-toxicity has been reported in numbers of incidence.

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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 Disilgold.com 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.

Sources
(*) Epigallocatechin gallate inhibits oxidative stress-induced DNA damage and
apoptosis in MRL-Fas(lpr) mice with autoimmune sialadenitis via upregulation
of heme oxygenase-1 and Bcl-2. by Saito K1, Mori S, Date F, Ono M.
(PubMed)
(*) EGCG attenuates autoimmune arthritis by inhibition of STAT3 and HIF-1α
with Th17/Treg control by Yang EJ1, Lee J2, Lee SY1, Kim EK1, Moon YM1,
Jung YO3, Park SH2, Cho ML1.(PubMed)
(*) Green tea EGCG, T cells, and T cell-mediated autoimmune diseases by Wu
D1, Wang J, Pae M, Meydani SN.(PubMed)
(*) The ability of green tea to alleviate autoimmune diseases: fact or fiction?
by Wu D, Wang J.