Saturday, 6 January 2018

Herbal Therapy: Green Tea and Lower Dose of Its Bioactive Polyphenols (-)-Epigallocatechin-3-gallate (EGCG) in Reduced Cardiac Fibrosis in Induction of Heart Failure

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

Green tea may have a therapeutic and positive effect in reduced risk and treatment of cardiac fibroids some scientists 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.

Cardiac fibrosis is a uncommon condition of abnormal thickening of the heart valves caused by inappropriate proliferation of cardiac fibroblasts but commonly, it is the excess deposition of molecules outside a cell or cells with structural and biochemical support to the surrounding cells in the cardiac muscle, leading to cardiac dysfunction and eventually heart failure.

The study of rat cardiac fibroblasts caused by injected by angiotensinII (AngII) also revealed that green tea inhibited the abnormal increase in level of connective tissue growth factor CTGF by decreased expression of the nuclear translocation of NF-κB p65 subunit and degradation of IκB-α in induced promotion of fibroblast proliferation and extracellular matrix (ECM) accumulation, thereby exacerbating cardiac hypertrophy and subsequent failure were attributed to bioactive polyphenol EGCG expression in significantly reduced collagen synthesis, fibronectin (FN) expression and cell proliferation.

In deed, due to the activity of CTGF as a matricellular protein modulating the fibrotic process in cardiac remodelling, some researchers suggested that the gowth factor may be considered as a biomarker for cardiac fibrosis for therapeutic intervention to mitigate fibrosis in the heart.

Interestingly, in the evaluated the effect of GABA tea, containing a high level of gamma-aminobutyric acid (GABA) in cardiac function with male Wistar rats injected with 55 mg/kg streptozotocin (STZ) to induce diabetes for 2 weeks and then orally given dosages of 4.55 and 45.5 mg/kg/day GABA tea extract for 6 weeks, researchers revealed that rats treated with injection of GABA tea not only induces fasting blood glucose levels returned to normal levels but also inhibits cardiac fibrosis in compared to untreated group.

Further experiments also showed that GABA tea in ameliorated cardiac deposit risk was attributed to inhibited the protein levels of tumor necrosis factor-alpha (TNF-alpha), Fas and activated caspase-8 and caspase-3 induced in STZ rats in mediated cardiomyocyte apoptosis which has been found in elevation in patient with cardiac dysfunction such as cardiac fibrosis and an indication of chronic hemodynamic overloading and early cardiac decompensation.

Dr. Cherng SH, the lead authors suggested," (GABA tea reduced)cardiac fibrosis (expression) in diabetic rats may be mediated by reducing blood glucose and further attenuating TNF-alpha expression and/or Fas/Fas ligand (FasL)-mediated apoptosis".

Unfortunately, injection of  bioactive polyphenols (-)-Epigallocatechin-3-gallate (EGCG) in high dose was found to induce the oppositely effect by increasing cardiac fibroids.

According to the study of green tea bioactive polyphenols (-)-Epigallocatechin-3-gallate (EGCG) in  risk of cardiac fibroids induction of myocardiotoxicity in animal model, at the the joint study lead by the Guangzhou Medical University, injection of EGCG 500 and 1000 mg/kg demonstrated a significant effect in initiated cardiac collagen synthesis involved in the formation of filtration systems, through cells differentiation in connective tissue growth factor (CTGF) mRNA expression and protein produced by fibroblasts.

Further more, the application of green tea extract also displayed an exhibited fibrosis-related protein expression in induction of cardiac fibroids deposit through stimulating function of fibronectin (FN), a ubiquitous extracellular matrix (ECM) glycoprotein circulated in the blood to initiated heart muscle repair.

After taking into account of other con confounders, Dr. Cai Y, the lead scientist said, "high oral doses of EGCG could induce cardiac fibrosis, and shed new light on the understanding of EGCG-mediated myocardiotoxicity".

The information findings suggested that green tea with bioactive poluphenols EGCG at lower dose may be used as function food in reduced risk of cardiovascular diseases caused by cardiac fibroids. In take of green tea supplement EGCG mus be taken with care as overdoses-toxicity has been reported in some cases.

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) GABA tea prevents cardiac fibrosis by attenuating TNF-alpha and Fas/FasL-mediated apoptosis in streptozotocin-induced diabetic rats by Cherng SH1, Huang CY2, Kuo WW3, Lai SE4, Tseng CY5, Lin YM6, Tsai FJ7, Wang HF8.(PubMed)
(2) High doses of (-)-epigallocatechin-3-gallate from green tea induces cardiac fibrosis in mice by Cai Y1, He SQ2, Hong HQ3, Cai YP4, Zhao L5, Zhang M2.(PubMed)
(3) EGCG inhibits CTGF expression via blocking NF-κB activation in cardiac fibroblast by Cai Y1, Yu SS, Chen TT, Gao S, Geng B, Yu Y, Ye JT, Liu PQ.(PubMed)

No comments:

Post a comment