scholarly journals Function of Green Tea Catechins in the Brain: Epigallocatechin Gallate and its Metabolites

2019 ◽  
Vol 20 (15) ◽  
pp. 3630 ◽  
Author(s):  
Monira Pervin ◽  
Keiko Unno ◽  
Akiko Takagaki ◽  
Mamoru Isemura ◽  
Yoriyuki Nakamura

Over the last three decades, green tea has been studied for its beneficial effects, including anti-cancer, anti-obesity, anti-diabetes, anti-inflammatory, and neuroprotective effects. At present, a number of studies that have employed animal, human and cell cultures support the potential neuroprotective effects of green tea catechins against neurological disorders. However, the concentration of (−)-epigallocatechin gallate (EGCG) in systemic circulation is very low and EGCG disappears within several hours. EGCG undergoes microbial degradation in the small intestine and later in the large intestine, resulting in the formation of various microbial ring-fission metabolites which are detectable in the plasma and urine as free and conjugated forms. Recently, in vitro experiments suggested that EGCG and its metabolites could reach the brain parenchyma through the blood–brain barrier and induce neuritogenesis. These results suggest that metabolites of EGCG may play an important role, alongside the beneficial activities of EGCG, in reducing neurodegenerative diseases. In this review, we discuss the function of EGCG and its microbial ring-fission metabolites in the brain in suppressing brain dysfunction. Other possible actions of EGCG metabolites will also be discussed.

2020 ◽  
Vol 21 (4) ◽  
pp. 1404 ◽  
Author(s):  
Yuchen Gu ◽  
Gautier Moroy ◽  
Jean-Louis Paul ◽  
Anne-Sophie Rebillat ◽  
Mara Dierssen ◽  
...  

Epigallocatechin gallate (EGCG) is an inhibitor of DYRK1A, a serine/threonine kinase considered to be a major contributor of cognitive dysfunctions in Down syndrome (DS). Two clinical trials in adult patients with DS have shown the safety and efficacy to improve cognitive phenotypes using commercial green tea extract containing EGCG (45% content). In the present study, we performed a preclinical study using FontUp®, a new nutritional supplement with a chocolate taste specifically formulated for the nutritional needs of patients with DS and enriched with a standardized amount of EGCG in young mice overexpressing Dyrk1A (TgBACDyrk1A). This preparation is differential with previous one used, because its green tea extract has been purified to up 94% EGCG of total catechins. We analyzed the in vitro effect of green tea catechins not only for EGCG, but for others residually contained in FontUp®, on DYRK1A kinase activity. Like EGCG, epicatechin gallate was a noncompetitive inhibitor against ATP, molecular docking computations confirming these results. Oral FontUp® normalized brain and plasma biomarkers deregulated in TgBACDyrk1A, without negative effect on liver and cardiac functions. We compared the bioavailability of EGCG in plasma and brain of mice and have demonstrated that EGCG had well crossed the blood-brain barrier.


2013 ◽  
Vol 53 (2) ◽  
pp. 793-800 ◽  
Author(s):  
Yanlan Xie ◽  
Agnieszka Kosińska ◽  
Hairong Xu ◽  
Wilfried Andlauer

2012 ◽  
Vol 6 (2) ◽  
pp. 73-93 ◽  
Author(s):  
Wendy W. Chen ◽  
Geng-Yao Qin ◽  
Ting Zhang ◽  
Wan-Yong Feng

2016 ◽  
Vol 311 (2) ◽  
pp. C308-C321 ◽  
Author(s):  
Li-Jane Shih ◽  
Tz-Fang Chen ◽  
Cheng-Kuo Lin ◽  
Hang-Shen Liu ◽  
Yung-Hsi Kao

Green tea catechins, especially (−)-epigallocatechin gallate (EGCG), have been reported to circulate in the placenta of animals and blood of humans after consumption. Whether EGCG regulates activity of human villous trophoblasts (HVT) is unknown. This study investigated the pathways involved in EGCG modulation of trophoblast mitogenesis. EGCG inhibited trophoblast proliferation in a dose-dependent and time-dependent manner, as indicated by the number of cells and incorporation of bromodeoxyuridine (BrdU). EGCG was more effective than other green tea catechins in inhibiting cell growth. EGCG also increased the phosphorylation of the MAPK pathway proteins, ERK1/2, and p38, but not JNK. Furthermore, EGCG had no effects on the total amounts of ERK1/2, p38 MAPK, and JNK proteins. This suggests that EGCG selectively affects particular MAPK subfamilies. Pretreatment with specific inhibitors of ERK1/2, p38 MAPK, and AMP-activated protein kinase (AMPK) antagonized EGCG-induced decreases in both cell number and BrdU incorporation. These inhibitors also blocked EGCG-induced increases in the levels of phospho-ERK1/2, phospho-p38, and phospho-AMPK proteins, respectively. Moreover, EGCG was similar to the phosphatidylinositol 3-kinase inhibitors wortmannin and LY-294002 to decrease protein kinase B (AKT) phosphorylation, cell number, and BrdU incorporation. These data imply that EGCG inhibits the growth of HVT through the ERK, p38, AMPK, and AKT pathways.


2021 ◽  
Vol 35 ◽  
Author(s):  
Maria Denise Rodrigues DE MORAES ◽  
Vanara Florêncio PASSOS ◽  
Gislaine Cristina PADOVANI ◽  
Lady Clarissa Brito da Rocha BEZERRA ◽  
Ilka Maria VASCONCELOS ◽  
...  

Author(s):  
Swarup Kumar Kundu ◽  
Shonkor Kumar Das ◽  
M. Sohidullah

Green tea obtained from the leaves of Camellia sinensis (L.) Kuntze having potential health benefits. It contains significant amounts of antioxidant and is considered as world healthiest drink. Polyphenols in tea are thought to exhibits anti-carcinogenic and anti-inflammatory effects. Green tea catechins acts as immune modulators in immune dysfunction and also play a role in protection from degenerative diseases. Intake of green tea catechins suppress high fat diet induced obesity, prevent lipid and glucose metabolism disorders and reduce risk of coronary heart disease. Green tea constituent epigallocatechin-3-gallate (EGCG) is a potential antioxidant that shows protective effects against photo toxicity and photo carcinogenesis. In vitro animal experiments have suggested that polyphenols in green tea protect from lung cancer by their antioxidant and antimutagenic properties. This study chiefly highlights the convenience of green tea on health and propagates its further prospects.


2012 ◽  
Vol 6 (2) ◽  
pp. 73-93 ◽  
Author(s):  
Wendy W. Chen ◽  
Geng-Yao Qin ◽  
Ting Zhang ◽  
Wan-Yong Feng

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