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Identification of a novel senomorphic agent, avenanthramide C, via SASP suppression

senescent cells senescence-associated secretory phenotype (sasp) avenanthramide c senomorphic

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#1 Engadin

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Posted 15 September 2020 - 01:32 PM


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P A Y W A L L E D   S O U R C E :   Mechanisms of Ageing and Development

 

 

 

 

 

 

Highlights
 
  •  Avn C lead a rescue of the senescence phenotypes.
 
  •  Avn C plays a different role in inhibiting NF-κB signaling between LPS-induced inflammation and inflammaging.
 
  •  Avn C can be a good candidate for the SASP modulator.
 
 
 
Abstract
 
Senescent cells are deeply involved in the induction of tissue damage and aging-related diseases. The identification of factors that eliminate senescent cells or inhibit the senescence-associated secretory phenotype (SASP) in these cells is necessary. Here, we report an avenanthramice C (Avn C) extracted from oat as a new SASP modulator.
 
Treatment with Avn C led to a significant reduction in the levels of markers of senescent cells, with no toxicity observed. The SASP was also inhibited by Avn C treatment, similar to non-senescent cells, and the suppression of cell division by autocrine signals associated with SASP was restored.
 
To investigate the mechanism underlying SASP inhibition by Avn C, we analyzed the effect of Avn C in lipopolysaccharide (LPS)-induced inflammation in non-senescent cells. Avn C inhibited nuclear factor κB (NF-κB) activity and the secretion of inflammatory cytokines before or after LPS treatment. Although the activity of MAP kinases, which are NF-κB upstream signals, was inhibited by Avn C in LPS-induced inflammation, only p38 activity was specifically inhibited in senescent cells. Interestingly, the inhibition of p38 in senescent cells was observed through Avn C-induced 5′-adenosine monophosphate-activated protein kinase (AMPK) activity. Avn C-induced inhibition of the SASP is triggered by senescence-related stress.
 
 
 
Outline
 
1. Introduction
 
2. Materials and methods
    2.1. Cell culture and Avn C treatment
    2.2. SA-β-Gal staining and quantitative assay
    2.3. Cytotoxicity assay
    2.4. Western blot analysis
    2.5. RNA isolation and quantitative real-time PCR (qPCR)
    2.6. Analysis of the levels of reactive oxygen species (ROS)
    2.7. Analysis of the SASP
    2.8. Cell growth analysis
    2.9. Analysis of NF-κB activity
    2.10. Statistical analysis
 
3. Results
    3.1. Senomorphic effects of Avn C on senescent phenotypes
    3.2. Suppression of the SASP by Avn C
    3.3. AMPK and p38 signaling involves in Avn C-dependent SASP modulation
 
4. Discussion
 
5. Conclusions
 
 
 
 
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Also tagged with one or more of these keywords: senescent cells, senescence-associated secretory phenotype (sasp), avenanthramide c, senomorphic

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