Wednesday 14 June 2023

#GreenTea's #Polyphenols #EGCG Improve Learning and Memory Deficits Through Their Anti Neuro-inflammatories Property, Researcher Find

By Kyle J. Norton

Green tea may have a therapeutic and positive effect in protecting against memory deficits, 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 "yin excessive syndrome" or "yang vacuity syndrome" including weakened immunity and painful case of GERD,... according to traditional Chinese medicine's Yin-Yang theory.

Memory deficit is a medical condition characterized by loss of the ability in-store and recall past information, such as knowledge, sensation, and thoughts,......

Loss of memory function is not only associated with normal aging progression in the adult population but is considered a feature of neurodegenerative diseases, including psychiatric and neurological disorders.

According to the Harvard neuro discovery center, today, approximately 5 million Americans suffer from Alzheimer's disease; 1 million from Parkinson's; 400,000 from multiple sclerosis (MS); 30,000 from amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease), and 30,000 from Huntington's disease.

The evaluate green tea extract (GTex) and its major functional polyphenol (−)-epigallocatechin gallate (EGCG) effect on the memory of cerebral ischemic rats showed that green tea EGCG and pentoxifylline (PTX), a methylxanthine derivative with anti-inflammatory function, application after 1 hour demonstrates strong efficacy in improved ischemia-induced memory impairment, according to Morris water maze test.

Long-term treatment of green tea EGCG also displayed a significant increase in levels of antioxidants such as malondialdehyde (MDA) levels, glutathione (GSH), and superoxide dismutase (SOD) activity in the cerebral cortex and hippocampus, through prevented cerebral infraction breakdown of MDA and GSH in the hippocampus, in protected against damage to cellular components caused by reactive oxygen species (ROS) including free radicals, peroxides, lipid peroxides...

Further analysis, green tea EGCG inhibited BV-2 microglial cells in the induction of brain inflammatory effect in precipitated neurodegeneration and neurotoxicology to facilitate memory impairment, through ameliorated the expression of lipopolysaccharide- (LPS-) in exhibited free radical nitric oxide production which is associated to in initiated neurotoxicity.

Additionally, the application also ameliorated the cyclooxygenase-2 (COX-2) expression associated with pro-inflammatory activities in mediated neurodegenerative processes of several acute and chronic diseases and expression of the inducible nitric oxide synthase (iNOS), one of the direct consequences of an inflammatory process in the BV-2 cells.

In short, the experiment of cerebral ischemia animal model indicated that green extract and its active polyphenol EGCG improved learning and memory deficits through exhibited antioxidant activity in the reduction of oxidative stress and neuroinflammation.

Moreover, green tea Epigallocatechin gallate (EGCG) with beneficial effects on the impairment of learning and memory also demonstrated increased autophagic activation in getting rid of damaged and dysfunctional cell accumulation to protect healthy neurons from stressful conditions, such as overexpression of ROS presentation, according to the experiment of chronic unpredictable mild stress (CUMS)-induced cognitive impairment in rats and observed through the elevated LC3-II, a reliable method for monitoring autophagy and autophagy-related processes, including autophagic cell death. and p62 protein level, a useful marker for the induction of autophagy,

At the same time, the green tea EGCG also displayed a strong inhibition of increased neuronal loss and activated mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6k) signaling caused by implication of chronic unpredictable mild stress (CUMS) in the CA1 regions in the hippocampal circuit in the initiation of the pathophysiology of memory deficits, thus reducing amyloid beta1-42 (Aβ1-42) deposit, and restored autophagic degradation activity.


The mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6k) signaling pathway is an essential cellular signaling pathway that involved a number of important physiological functions, including cell growth, proliferation, metabolism, protein synthesis, and autophagy.

Taken together, green tea and its bioactive polyphenols Epigallocatechin gallate (EGCG) may be considered an adjunct therapy in reduced risk and enhanced standard medicine for the treatment of memory deficits.


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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 the international journal Pharma and Bioscience, ISSN 0975-6299.


Sources
(1) Green Tea Extract Ameliorates Learning and Memory Deficits in Ischemic Rats via Its Active Component Polyphenol Epigallocatechin-3-gallate by Modulation of Oxidative Stress and Neuroinflammation by Kuo-Jen Wu,1 Ming-Tsuen Hsieh,1 Chi-Rei Wu,1 W. Gibson Wood,2 and Yuh-Fung Chen(Hindawi)
(2) Epigallocatechin-3-Gallate Attenuates Impairment of Learning and Memory in Chronic Unpredictable Mild Stress-Treated Rats by Restoring Hippocampal Autophagic Flux by Hong-Feng Gu1,2., Ya-Xiong Nie3., Qiao-Zhen Tong2., Ya-Ling Tang1 , Yang Zeng3 , Kai-Quan Jing3 , XiLong Zheng2,4, Duan-Fang Liao4(PLOS 1)

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