Green Tea Bioactive Epigallo-catechin-3-gallate (EGCG) in Reduced Risk, Progression and Treatment of and Neuro-Degenerative Diseases

Green tea is found to consist of substantial and respectful effect in reduced risk, progression, and treatment of neurodegenerative diseases, some scientists opinionated.


Neurodegenerative diseases are a class of conditions characterized by deteriorating neurons and accumulated plaque in blocking the neurotransmitters of the brain and spinal cords in performance of normal functions.

According to the statistic, approximately, 5 million Americans suffer from Alzheimer's disease, 1 million from Parkinson's and 400,000 from multiple sclerosis (MS) today, inducing overwhelming social, economic and health care burden on society.



The differentiation of green tea bioactive constituents in the risk of neuro-degenerative diseases was found to associate to numbers of the mechanism through many different aspects.


The investigation of green tea bioactive epigallocatechin-gallate (EGCG) activities in lipopolysaccharide- (LPS-) mediated systemic inflammation in the induction of neurodegenerative diseases suggested that application of green tea chemical constituent demonstrated a significant effect in ameliorated LPS induced expression of proinflammatory cytokines of tumor necrosis factor alpha TNF-α, a cell signaling protein involved in systemic inflammation in the acute phase of infection, and interleukin 1 beta (IL1β), an cytokine with function in the regulation of immune and inflammatory responses to infections or sterile insults and interleukin 6 (IL-6) involved in inflammation and infection responses, particularly, in the inhibition of the expressions of inflammatory cytokines in the mononuclear blood cells (PBMCs), consisting lymphocytes (T cells, B cells, NK cells) with function to clear away of debris in the infection site.

The activation of inflammatory cytokines expression caused by lipopolysaccharide- (LPS) injection can trigger neurotoxicity, leading to neurons brains progressive degeneration, resulting in elevated risk of neurodegenerative diseases.

Application of green tea bioactive epigallocatechin-gallate (EGCG) was found not only inhibited LPS in precipitation of toxicity in resolved inflammation and mediated neuroprotection but also exerted anti toxicity through its antioxidant activity in decreased expression of reactive oxygen species in triggered brain cell apoptosis.


Interleukin 6 (IL-6) acts as both pro-inflammatory cytokines and anti-inflammatory cytokines with function involved inflammation responses at sites of acute and chronic infection.

Further analysis of green tea Epigallocatechin-3-gallate (EGCG) in the aspect of ROS in risk of neurodegeneration in the dentate gyrus, part of the hippocampus and/or hippocampal formation of C57Bl/6 mice, suggested that the application promoted neural precursor cell, (a partially differentiated cell) proliferation, without changes at the level of immature and mature new neurons.



Interestingly, in adult hippocampal neurogenesis in male Balb/C mice, injection of green tea bioactive compounds in different doses also expressed a strong implication of increased cells survival without affecting cell proliferation but decreasing apoptotic cells.

The increased production of neuro precursor cell in stimulated neuron generation and increased cell survival from green tea was attributed to the green tea antioxidants acted as free radical scavengers to ameliorate chain reaction stimulated by reactive oxygen species (ROS).


Furthermore, green tea treatment was found to promote the production of more elaborated dendritic (structures on the neuron that receive electrical messages) trees in young DCX-positive neurons with function in the acquisition of spatial learning, as well as reversal learning, but not the retrieval of stored long-term memories.


The implication of green tea bio compounds EGCG also significantly increased net growth and development of nervous tissue in the adult hippocampus and hippocampal levels of phospho-Akt.in regulated multiple cellular processes, including glucose metabolism, apoptosis, cell proliferation, transcription, and cell migration by re-establishing the function of PI3K in the intracellular signaling pathway.

Dr. Neha Atulkumar Singh, the lead author in the article of "Potential neuroprotective properties of epigallocatechin-3-gallate (EGCG)", said, "there is a need to identify a class of drug capable of reversing neural damage and preventing further neural death" and "assesses the reliability of the neuroprotective benefits of epigallocatechin-gallate (EGCG) by shedding light on their biological, pharmacological, antioxidant and metal chelation properties, with emphasis on their ability to invoke a range of cellular mechanisms in the brain".


Taken together, green bioactive compound, EGCG may represent a potent and useful neuroprotective agent for inflammation-mediated neurological disorders and be considered as a useful principle in modulated brain plasticity.


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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
(2) Potential neuroprotective properties of epigallocatechin-3-gallate (EGCG).
Singh NA1, Mandal AK2, Khan ZA3.(PubMed)
(*) Neuroprotective Activity of (-)-Epigallocatechin Gallate against Lipopolysaccharide-Mediated Cytotoxicity by Liu JB1, Zhou L1, Wang YZ2, Wang X2, Zhou Y2, Ho WZ3, Li JL2.(PubMed)
(*) Green tea compound epigallo-catechin-3-gallate (EGCG) increases neuronal survival in adult hippocampal neurogenesis in vivo and in vitro by Ortiz-López L1, Márquez-Valadez B2, Gómez-Sánchez A1, Silva-Lucero MD3, Torres-Pérez M1, Téllez-Ballesteros RI1, Ichwan M4, Meraz-Ríos MA5, Kempermann G6, Ramírez-Rodríguez GB7.(PubMed)