We are analyzing https://link.springer.com/article/10.1007/s12602-019-09576-z.

Title:
Cell-Free Culture Supernatant of Probiotic Lactobacillus fermentum Protects Against H2O2-Induced Premature Senescence by Suppressing ROS-Akt-mTOR Axis in Murine Preadipocytes | Probiotics and Antimicrobial Proteins
Description:
Information regarding cellular anti-senescence attributes of probiotic bacteria vis-à-vis modulation of senescence-associated secretory phenotype (SASP) and mTOR signaling is very limited. The present study assessed anti-senescence potential of secretory metabolites of probiotic Lactobacillus fermentum (Lact. fermentum) using H2O2-induced model of senescence in 3T3-L1 preadipocytes. Application of H2O2-induced cellular senescence characterized by increased cell size and SA-β-gal activity, activation of SASP and reactive oxygen species (ROS), DNA damage response and induction of cell cycle inhibitors (p53/p21WAF1/p16INK4a). Further, a robust stimulation of the PI3K/Akt/mTOR pathway and AMPK signaling was also observed in H2O2-treated cells. However, exposure of cells to cell-free supernatant of Lact. fermentum significantly attenuated phosphorylation of PI3K/Akt/mTOR pathway and alleviated senescence markers p53, p21WAF1, SA-β-gal, p38MAPK, iNOS, cox-2, ROS, NF-κB, and DNA damage response. These results provide evidence that secretory metabolites of Lact. fermentum can mitigate the development as well as severity of stress-induced senescence thereby indicating its utility for use as anti-aging or age-delaying agent.
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article, google, scholar, pubmed, cas, senescence, central, cell, sharma, aging, lactobacillus, probiotics, probiotic, cells, fermentum, httpsdoiorg, cellular, secretory, response, pathway, httpsdoiorgs, kumar, padwad, mtor, mice, human, gut, cancer, premature, gupta, sasp, signaling, pikaktmtor, oxidative, food, stress, wang, lee, privacy, cookies, content, information, preadipocytes, activation, nfκb, access, induces, inflammation, nature, med,

Topics {✒️}

atm-dependent nf-κb activation suppressing ros-akt-mtor axis cell-free culture supernatant month download article/chapter reactive oxygen species pi3k/akt/mtor pathways pi3k/akt/mtor pathway th1/th2 immune homeostasis p38-induced cellular senescence cellular anti-senescence attributes h2o2-induced premature senescence author information authors wnt/ β-catenin pathways mucin-degrading akkermansia muciniphila probiotic lactobacillus fermentum gc-rich promoter elements nf-κb promotes senescence csir-ihbt publication number systemic inflammatory response sa-β-gal activity lactobacillus fermentum hfb3 lactobacillus pentosus var stress-induced senescence potential probiotic strain phytochemical epigallocatechin gallate cell-free supernatant antimicrobial proteins aims oxidation-inflammation theory mitochondrial stress response aberrant mtor activation full article pdf lactobacillus casei shirota p38 map-kinase bax/bcl-2 pathway mtor-mediated signaling article kumar anamika sharma cellular damage induced age-related diseases privacy choices/manage cookies oncogenic premature senescence sa-β-gal oncogene-induced senescence h2o2-induced model p53/p21waf1/p16ink4a van de sluis de souza sr age-related disease cellular senescence induction activated murine macrophages

Questions {❓}

Birch J, Passos JF (2017) Targeting the SASP to combat ageing: mitochondria as possible intracellular allies?
Borodkina AV, Deryabin PI, Giukova AA, Nikolsky NN (2018) “Social Life” of senescent cells: what is SASP and why study it?
Nacarelli T, Azar A, Sell C (2015) Aberrant mTOR activation in senescence and aging: a mitochondrial stress response?

Schema {🗺️}

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         description:Information regarding cellular anti-senescence attributes of probiotic bacteria vis-à-vis modulation of senescence-associated secretory phenotype (SASP) and mTOR signaling is very limited. The present study assessed anti-senescence potential of secretory metabolites of probiotic Lactobacillus fermentum (Lact. fermentum) using H2O2-induced model of senescence in 3T3-L1 preadipocytes. Application of H2O2-induced cellular senescence characterized by increased cell size and SA-β-gal activity, activation of SASP and reactive oxygen species (ROS), DNA damage response and induction of cell cycle inhibitors (p53/p21WAF1/p16INK4a). Further, a robust stimulation of the PI3K/Akt/mTOR pathway and AMPK signaling was also observed in H2O2-treated cells. However, exposure of cells to cell-free supernatant of Lact. fermentum significantly attenuated phosphorylation of PI3K/Akt/mTOR pathway and alleviated senescence markers p53, p21WAF1, SA-β-gal, p38MAPK, iNOS, cox-2, ROS, NF-κB, and DNA damage response. These results provide evidence that secretory metabolites of Lact. fermentum can mitigate the development as well as severity of stress-induced senescence thereby indicating its utility for use as anti-aging or age-delaying agent.
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      description:Information regarding cellular anti-senescence attributes of probiotic bacteria vis-à-vis modulation of senescence-associated secretory phenotype (SASP) and mTOR signaling is very limited. The present study assessed anti-senescence potential of secretory metabolites of probiotic Lactobacillus fermentum (Lact. fermentum) using H2O2-induced model of senescence in 3T3-L1 preadipocytes. Application of H2O2-induced cellular senescence characterized by increased cell size and SA-β-gal activity, activation of SASP and reactive oxygen species (ROS), DNA damage response and induction of cell cycle inhibitors (p53/p21WAF1/p16INK4a). Further, a robust stimulation of the PI3K/Akt/mTOR pathway and AMPK signaling was also observed in H2O2-treated cells. However, exposure of cells to cell-free supernatant of Lact. fermentum significantly attenuated phosphorylation of PI3K/Akt/mTOR pathway and alleviated senescence markers p53, p21WAF1, SA-β-gal, p38MAPK, iNOS, cox-2, ROS, NF-κB, and DNA damage response. These results provide evidence that secretory metabolites of Lact. fermentum can mitigate the development as well as severity of stress-induced senescence thereby indicating its utility for use as anti-aging or age-delaying agent.
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