We are analyzing https://link.springer.com/article/10.1007/s10522-018-9785-1.

Title:
Epigallocatechin gallate suppresses premature senescence of preadipocytes by inhibition of PI3K/Akt/mTOR pathway and induces senescent cell death by regulation of Bax/Bcl-2 pathway | Biogerontology
Description:
The phytochemical epigallocatechin gallate (EGCG) has been reported to alleviate age-associated immune disorders and organ dysfunction. However, information regarding the mechanistic role of EGCG in the suppression of cellular senescence is limited. The present study thus assessed the effects and underlying mechanisms of EGCG in the inhibition of senescence as well as its potential to selectively eliminate senescent cells (senolytics) using 3T3-L1 preadipocytes. Premature senescence was established in cells by repeated exposure of H2O2 at a sub-lethal concentration (150 μM). H2O2 treated cells showed characteristic senescence-associated features including increased cell size, senescence-associated β-galactosidase activity (SA-β-gal), development of senescence-associated secretory phenotype (SASP), activation of reactive oxygen species (ROS) and pathways, DNA damage as well as induction of cell cycle inhibitors (p53/p21WAF1/p16INK4a). In addition, a robust activation of PI3K/Akt/mTOR and AMPK pathways was also observed in H2O2 treated cells. Presence of EGCG (50 and 100 μM) showed significant downregulation of PI3K/Akt/mTOR and AMPK signaling along with the suppression of ROS, iNOS, Cox-2, NF-κB, SASP and p53 mediated cell cycle inhibition in preadipocytes. In addition, EGCG treatment also suppressed the accumulation of anti-apoptotic protein Bcl-2 in senescent cells thereby promoting apoptosis mediated cell death. Our results collectively show that EGCG acts as an mTOR inhibitor, SASP modulator as well as a potential senolytic agent thereby indicating its multi-faceted attributes that could be useful for developing anti-aging or age-delaying therapies.
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Keywords {🔍}

pubmed, article, google, scholar, cas, senescence, cell, aging, central, egcg, cells, sharma, cellular, premature, senescent, ros, secretory, mtor, med, kim, privacy, cookies, content, biogerontology, preadipocytes, pikaktmtor, pathway, kumari, effects, access, chen, oxidative, lee, author, information, publish, research, search, epigallocatechin, gallate, inhibition, kumar, padwad, immune, senescenceassociated, sasp, activation, apoptosis, inflammation, stress,

Topics {✒️}

nuclear factor kappa-light-chain-enhancer suppressing ros-akt-mtor axis month download article/chapter author information authors h2o2-induced premature senescence potential senolytic agent pi3k/akt/mtor pathway mtorc1/autophagy axis ros-mediated cellular signaling amita kumari anti-apoptotic protein bcl-2 anamika sharma article kumar age-dependent behavioral declines phytochemical epigallocatechin gallate pi3k/akt/mtor full article pdf cell cycle inhibitors article biogerontology aims epigallocatechin-3-o-gallate bax/bcl-2 pathway humoral immune responses oncogenic premature senescence hpa axis functions rohit sharma aberrant mtor activation significant longevity-extending effects β-galactosidase activity privacy choices/manage cookies h2o2 treated cells aging cells-connecting metabolism showed significant downregulation check access finding shangri-la yogendra padwad instant access mesenchymal stem cells reactive oxygen species natural antioxidants egcg sirt1-dependent pathway protein-dye binding 3t3-l1 preadipocytes cell cycle 7 sa-β-gal related subjects human dermal fibroblasts epigallocatechin-3-gallate age-related diseases cellular senescence induction mitochondrial stress response

Questions {❓}

Nacarelli T, Azar A, Sell C (2015) Aberrant mTOR activation in senescence and aging: a mitochondrial stress response?

Schema {🗺️}

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         description:The phytochemical epigallocatechin gallate (EGCG) has been reported to alleviate age-associated immune disorders and organ dysfunction. However, information regarding the mechanistic role of EGCG in the suppression of cellular senescence is limited. The present study thus assessed the effects and underlying mechanisms of EGCG in the inhibition of senescence as well as its potential to selectively eliminate senescent cells (senolytics) using 3T3-L1 preadipocytes. Premature senescence was established in cells by repeated exposure of H2O2 at a sub-lethal concentration (150 μM). H2O2 treated cells showed characteristic senescence-associated features including increased cell size, senescence-associated β-galactosidase activity (SA-β-gal), development of senescence-associated secretory phenotype (SASP), activation of reactive oxygen species (ROS) and pathways, DNA damage as well as induction of cell cycle inhibitors (p53/p21WAF1/p16INK4a). In addition, a robust activation of PI3K/Akt/mTOR and AMPK pathways was also observed in H2O2 treated cells. Presence of EGCG (50 and 100 μM) showed significant downregulation of PI3K/Akt/mTOR and AMPK signaling along with the suppression of ROS, iNOS, Cox-2, NF-κB, SASP and p53 mediated cell cycle inhibition in preadipocytes. In addition, EGCG treatment also suppressed the accumulation of anti-apoptotic protein Bcl-2 in senescent cells thereby promoting apoptosis mediated cell death. Our results collectively show that EGCG acts as an mTOR inhibitor, SASP modulator as well as a potential senolytic agent thereby indicating its multi-faceted attributes that could be useful for developing anti-aging or age-delaying therapies.
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