Tuesday 13 February 2018

Herbal Therapy: Green tea and its Bioactive Pophenol EGCG in Attenuated Oxidative Stress in Facilitated Fibromyalgia

Kyle J. Norton 

Green tea may have a therapeutic and positive effect in reduced risk, progression and treatment of
fibromyalgia caused by oxidative stress, some scientists suggested.

Green tea, a precious drink processes numbers of health benefit known to almost everyone in Asia and Western world.

Fibromyalgia (FM) is a chronic condition characterized by muscle and soft tissue pain affecting over 10 million (3.6% of the population) people in US alone.

According to the study in review of literature of the frequency and pattern of complementary and alternative medicine (CAM) of 289(95%)  patients who completed the survey (263 women and 26 men) between February 2003 and July 2003, green tea was recommended at 24% for treatment of  fibromyalgia (FM).

In other words, in herbal medicine, green tea is considered to have certain effect in reduced symptoms and treatment for such syndrome.

Some evidences in medical literature suggested that over production of ROS in induction of oxidative stress may have a strong implication in the pathophysiology of FM.

In the investigation of the effect of green tea epigallocatechin-3-gallate (EGCG) in protection of oxidative stress to cardiac cells cultured in the conditions of control, 400 μM H2O2 exposure for 30 min with and/or without 10 to 20 μM EGCG pre-treatment, researchers at the National Tsing Hua University found that treatment of green tea in H(2)O(2) group demonstrated a significant reduction of levels of reactive oxygen species through its antioxidant and its ability in induced production of natural antioxidant presented in the cardiac cells in compared to over expression of ROS in H2O2 treatment group without injection of EGCG.

Also, application of green tea reduced levels of cytosolic Ca2+ overload in the H(2)O(2) group in induced oxidative stress in experiment cell apoptosis through improved antioxidant protein.

Interestingly, EGCG inhibited the ameliorated H(2)O(2) expression in increased glycolytic protein in response to the degree of oxidative stress in the culture cells and α-enolase, a key glycolytic enzyme on the surface of several cell types in contribution of impaired glycolytic activity through oxidative and nitrative stress.

Additionally, green tea EGCG also decreased levels of peroxiredoxin-4, an antioxidant with function in protection against oxidative stress by detoxifying peroxides and mitochondrial proteins with function of redox reactions of oxidative phosphorylation.

After taking into account of other con founders, researchers suggested that ingestion of green tea EGCG inhibited the damage of H(2)O(2) group through inhibition of the downstream signalling for Akt in expression glucose oxidation and cell apoptosis in cellular processes, and loss of phosphorylation of GSK-3β and cyclin D1 depletion in facilitated oxidative stress.

These result postulated that green tea EGCG exerted the similar inhibited effect of those of GSK-3β inhibitor (SB 216763) in significantly improved H(2)O(2)-induced suppression on cell viability, phosphorylation of pAkt (S473) and pGSK-3β (S9), and level of cyclin D1 in cells.

The above differentiation was supported by the study conducted by the Universidad de Sevilla, in evaluated some evidences of green tea in reduced oxidative stress in facilitated pathophysiology of FM in initiated signs and symptoms of muscular alteration and mitochondrial dysfunction.

Truly, in primary rat model, administration of green tea EGCG in different concentrations for 24 h before being exposed to hydrogen peroxide (H(2)O(2)) for 2 h to induce oxidative stress, researchers found that pretreatment with 10, 25, and 50 µM EGCG significantly inhibited the expression of H2O2 in reduced substantial decrease in cell viability.

Further analysis also showed that green EGCG application dose of 50 µM ameliorated the proportion of propidium iodide (PI)-positive cells increased in cultures caused by H(2)O(2) injection, thus reducing H(2)O(2) in induced cell death.

Taken together, green tea and its bioactive polyphenols EGCG may be considered as a functional food in reduced risk, progression and treatment of fibromyalgia caused by over expression of oxidative stress. However, in take of green tea supplement should be taken with extreme care as acute liver toxicity has been reported in numbers of medical literature.

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


Back to Kyle J. Norton Home page http://kylejnorton.blogspot.ca

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
(1) Use of complementary and alternative medical therapies by patients referred to a fibromyalgiatreatment program at a tertiary care center by Wahner-Roedler DL1, Elkin PL, Vincent A, Thompson JM, Oh TH, Loehrer LL, Mandrekar JN, Bauer BA.(PubMed)
(2) Oxidative stress and mitochondrial dysfunction in fibromyalgia by Cordero MD1, de Miguel M, Carmona-López I, Bonal P, Campa F, Moreno-Fernández AM(PubMed)Molecular identification for epigallocatechin-3-gallate-mediated antioxidant intervention on the H2O2-induced oxidative stress in H9c2 rat cardiomyoblasts by Chen WC, Hsieh SR, Chiu CH, Hsu BD1, Liou YM.(PubMed)
(3) Molecular identification for epigallocatechin-3-gallate-mediated antioxidant intervention on the H2O2-induced oxidative stress in H9c2 rat cardiomyoblasts by Chen WC, Hsieh SR, Chiu CH, Hsu BD1, Liou YM.(PubMed)

No comments:

Post a Comment