Thursday, September 26, 2019

Green Tea and its Bioactive Polyphenol Epigallocatechin 3-gallate (EGCG) in Alleviated Symptoms, Reduced Risk, Progression and Treatment of Arthritis

Green tea may have a therapeutic and positive effect in reduced risk and progression and treatment of arthritis, some scientists suggested.

Arthritis is a chronic condition characterized by painful inflammation and stiffness of the joints.

According to statistic, arthritis is the common autoimmune disorder affected over 50 million worldwide.

According to the College of Pharmacy, green tea epigallocatechin 3-gallate (EGCG) in preclinical studies displayed a significant effect in the treatment of arthritic disease.

In vitro, the application of green tea extract EGCG demonstrated activities in cartilage-preserving and chondroprotective action through reduced expression of proinflammatory IL-1β, TNFα, and IL-6
and modulated extracellular matrix (ECM) turnover induced changes of the biomechanical environment of chondrocytes and accelerate the degradation of cartilage as well as driving the progression of the disease in the presence of inflammation.

Normal extracellular matrix (ECM) is a composed collagen type II with function to provide tensile support for the tissue.

Further analysis in the expression of proinflammatory factors researchers found that the overexpression of proinflammatory cytokines IL-1 and IL-6 were associated correlatively in knee joints in arthritis and inhibition of IL-1 and IL-6 by green tea EGCG IL-1 showed to reduce joint damage.

Some researchers also suggested that Interleukin 1 (IL-1) is a crucial mediator of the inflammatory response, playing an important part in the body's natural responses and the development of pathological conditions leading to chronic inflammation.

In the expression of tumor necrosis factor (TNF), tumor necrosis factor-alpha(TNFα, cachexin, or cachectin), application of green tea inhibited the levels of TNFα in the induction of synovial fibroblast cytotoxicity.

Interestingly, in the study to evaluate the possible effects of the administration of green tea extract on the oxidative state of the liver and brain of adjuvant-induced arthritic rats, researchers indicated that green tea daily doses of 250 mg kg(-1) (59.8 mg catechins per kg) for 23 days displays a strong effect in decreased symptoms of arthritis by ameliorated diminutions in protein and lipid damage in liver, brain and plasma, through antioxidant effect in reduced levels of ROS in stimulated free radical chain reaction to initiate production of pro-inflammatory cytokines to precipitate chronic diseases.

Rats treated with green tea EGCG also showed a significant improvement in restored natural antioxidant glutathione (GSH) and protein thiol levels produced by the body, by exhibiting the activities of the antioxidant enzymes.

Moreover, green tea injection also normalized the activity of glucose 6-phosphate dehydrogenase, which is increased in the liver of arthritic patients and considered as a risk factor for the development of arthritis. Increased activity glucose 6-phosphate dehydrogenase was associated to reactive oxygen species (ROS) generated in oxidative metabolism in inflicted damage on all classes of macromolecules.

Additional differentiation of green tea EGCG immunomodulatory effects and mechanisms on experimental arthritis induced by collagen-induced arthritis (CIA) in mice in compared to control received phosphate-buffered saline (PBS), researchers found that application of green tea EGCG at dose of 10 mg/kg demonstrated a strong effect in ameliorated clinical symptoms and reduced histological scores in arthritic mice, through modulated the immune activity by induced overexpression of the Nrf-2 antioxidant pathway, a major mechanism in the cellular defense against oxidative or electrophilic stress through detoxication and elimination.

EGCG also ameliorated experimental arthritis in mice by eliciting indoleamine-2,3-dioxygenase (IDO) through inhibition of pro-inflammatory cytokine interferon-gamma, astrocytes and microglia in facilitated production of dendritic cells (DCs) in the activation of the immune system to attack the dendritic cell located on the surface on the joint tissue.

Application of the EGCG also increased frequencies of T regs with a dominant role in the suppression of autoimmune pathology.

Some researchers suggested that increased Treg number and/or function in model systems may have a significant effect on both prevented and reversed arthritis disease.

Taken together, green tea with abundant bioactive polyphenol epigallocatechin 3-gallate (EGCG) may be considered as a functional food for alleviated symptoms, reduced risk, and progression and treatment of arthritis.

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Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, 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 Bioscience, ISSN 0975-6299.

Sources
(1) Green tea extract improves the oxidative state of the liver and brain in rats with adjuvant-induced arthritis by de Almeida Gonçalves G1, de Sá-Nakanishi AB, Wendt MM, Comar JF, Bersani Amado CA, Bracht A, Peralta RM.(PubMed)
(2) Green Tea Epigallocatechin-3-Gallate Suppresses Autoimmune Arthritis Through Indoleamine-2,3-Dioxygenase Expressing Dendritic Cells and the Nuclear Factor, Erythroid 2-Like 2 Antioxidant Pathway by Min SY1, Yan M1, Kim SB2, Ravikumar S1,3, Kwon SR1,4, Vanarsa K1,3, Kim HY4, Davis LS#1, Mohan C(PubMed)
(3) Green tea polyphenol epigallocatechin 3-gallate in arthritis: progress and promise by Ahmed S1.(PubMed)
(4) Is IL-1 a good therapeutic target in the treatment of arthritis? by Burger D1, Dayer JM, Palmer G, Gabay C.(PubMed)

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