Green tea may have a therapeutic and positive effect in reduced risk and treatment of atherosclerosis, some scientists suggested.
Green tea, a precious drink processes a number of health benefits known to almost everyone in Asia and the Western world. However, as yin in nature herbal medicine or food, long-term injection of large amounts may obstruct the balance of yin-yang, inducing "excessive yin syndrome" or "yang vacuity syndrome" including weakened immunity and painful case of GERD,... according to traditional Chinese medicine's Yin-Yang theory.
Atherosclerosis is medical condition characterized by the deposition of plaques of fatty material on the inner walls, causing to hardening of the arterial vessels.
According to statistics, the mortality rate of coronary heart disease was about 60% in 2010 compared to 30% for stroke and heart failure.
In the study to determine the effect of green tea bioactive epigallocatechin-3-gallate (EGCG) in ameliorated Porphyromonas gingivalis -induced atherosclerosis in a murine model, after injection of the extract EGCG, the tested mice than fed high-fat diets and injected with P. gingivalis three times a week for 3 weeks, observation at weeks 15 displayed a significant reduction of atherosclerotic plaques accumulated in the branches of arteries, observed by Oil Red O staining
Further analysis also found that the polyphenol extract decreased infection of atherosclerotic lesion areas in the anatomic dilations of the ascending aorta through decreased expression of C-reactive protein, in regulating the acute phase of infection and monocyte chemoattractant protein-1 (MCP-1/CCL2) chemokines in regulated migration and infiltration of monocytes/macrophages. of the immune system in induced production of cytokines to counter foreign substances.
Additional observation, also indicated that green tea bioactive epigallocatechin-3-gallate (EGCG) not also improved LDL/very LDL cholesterol but also ameliorated ROS activity via antioxidant in induced low-density lipoprotein (LDL) oxidation, a leading indicator of plague accumulation.
In depth differentiation, the efficacy of green tea epigallocatechin-3-gallate (EGCG) in reduced expression of atherosclerosis due to bacterial P. gingivalis was attributed to decrease secreted proteins with functions in stimulated inflammatory effects, such as chemokines (CCL2) involved in immunoregulatory and inflammatory processes, matrix metallopeptidase 9 (MMP-9) in regulated pathological remodeling processes that involve inflammation, ICAM-1 (Intercellular Adhesion Molecule 1) involvesd inflammation of capillary vessel walls, the mitochondrial chaperonin hsp60 in induction of inflammation,......
Interestingly, in the process to prevent plague to initiation of development of atherosclerosis through above implications, green tea epigallocatechin-3-gallate (EGCG) also increased levels of antioxidant defense enzyme (heme oxygenase-1 mRNA) HO-1 mRNA levels in reduced expression of oxidative stress in induction of pathogenic inflammatory diseases.
Intrusively, continued investigation the effect of epigallocatechin-3-gallate (EGCG) in inhibiting the formation and development of atherosclerosis via its anti-inflammatory capability also found that EGCG restricts the function of IL6 (interleukin 6) in induced over-expression of pro-inflammatory cytokines and Angiotensin (Ang) II functions in stimulated and increased vascular permeability through production of vascular endothelial cell growth factor CRP in initiated the pro-inflammatory process.
Interleukin 6 is an interleukin with duo functions of pro inflammatory cytokines and anti-inflammatory cytokines.
Amazingly, antioxidant activities of EGCG also acted as free radical scavengers to prevent ROS to establish a chain reaction in induction of inflammatory effect in encouraging lipid accumulation in the inner wall of arteries, the leading cause of atherosclerosis.
ROS are free radicals with the function to mediate many pathophysiological processes, such as growth, migration, apoptosis and secretion of inflammatory cytokines,
Angiotensin is a hormone with function in regulated vasoconstriction in increased blood pressure.
Application of combined (-)-Epigallocatechin gallate (EGCG) +chitosan (CS) and aspartic acid (PAA). demonstrated a significant effect in reduced risk and treatment of atherosclerosis through ameliorated lipid deposition in tested animals.
In comparison to the effects of conventional medicine simvastatin with an approximately successful treatment rate of lipid deposition of 15.6%, injection of (-)-Epigallocatechin gallate (EGCG) +chitosan (CS) and aspartic acid (PAA).exhibited overall treatment rate of 16.9%.
The evidence suggests that EGCG, as a natural substance, may have a substantial and therapeutic effect in attenuating the risk and treatment of atherosclerosis through anti-inflammatory and antioxidative activities.
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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 online, including worldwide health, ezine articles, article base, healthblogs, 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 the international journal Pharma and Bio Science, ISSN 0975-6299.
Sourcesase
(1) Green tea epigallocatechin-3-gallate attenuates Porphyromonas gingivalis -induced atherosclerosis by Yu Cai Tomoko Kurita-Ochiai Tomomi Hashizume Masafumi Yamamoto(Pathogen and Disease)
https://academic.oup.com/femspd/article/67/1/76/2367414
(2) Improving the effectiveness of (-)-epigallocatechin gallate (EGCG) against rabbit atherosclerosis by EGCG-loaded nanoparticles prepared from chitosan and polyaspartic acid by Hong Z1, Xu Y, Yin JF, Jin J, Jiang Y, Du Q.(PubMed)
(3) Epigallocatechin-3-gallate inhibits interleukin-6- and angiotensin II-induced production of C-reactive protein in vascular smooth muscle cells by NingPeng, Jun-tian Liu Fang. Guo. Rui Li(Science Direct)
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