Ginsenoside F1 suppresses astrocytic senescence-associated secretory phenotype

Cited 4 time in webofscience Cited 0 time in scopus
  • Hit : 176
  • Download : 0
Senescence is one of the hallmarks of aging and identified as a potential therapeutic target in the treatment of aging and aging-related diseases. Senescent cells accumulate with age in a variety of human tissues where they develop a complex senescence-associated secretory phenotype (SASP). SASP in brain could contribute to age-related inflammation and chronic neurodegenerative diseases. We confirmed that senescent astrocytes express a characteristic of SASP in vitro by human cytokine antibody array. Ginsenoside F1 suppresses the SASP from astrocytes induced by D-galactose via suppressing p38MAPK-dependent NF-kappa B activity. A specific inhibitor of p38MAPK, SB203580 significantly decreased the secretion of IL-6 and IL-8, the major components of SASPs. Additionally, treatment of senescent astrocytes with NF-kappa B inhibitor, BAY 11-7092, also suppressed the secretion of IL-6 and IL-8, suggesting NF-kappa B was required for SASP. Importantly, conditioned media from senescent astrocytes promoted the migration of glioblastoma cells, such as U373-MG, U251-MG and U87-MG assessed by scratch wound healing. This migration was significantly decreased by F1 treatment in senescent astrocytes. Interestingly, IL-8, the main mediator regulating glioblastoma cell invasion, was suppressed in both transcriptional and protein level. Herein, we propose ginsenoside F1 as a potential therapeutic strategy for reducing the deleterious contribution of senescent astrocytes in aged brain and related diseases.
Publisher
ELSEVIER IRELAND LTD
Issue Date
2018-03
Language
English
Article Type
Article
Keywords

DNA-DAMAGE RESPONSE; INFLAMMATORY CYTOKINE SECRETION; AGING-RELATED DISEASE; CELLULAR SENESCENCE; OXIDATIVE STRESS; KAPPA-B; EXPRESSION; BRAIN; MICE; PROLIFERATION

Citation

CHEMICO-BIOLOGICAL INTERACTIONS, v.283, pp.75 - 83

ISSN
0009-2797
DOI
10.1016/j.cbi.2018.02.002
URI
http://hdl.handle.net/10203/240923
Appears in Collection
BS-Journal Papers(저널논문)BiS-Journal Papers(저널논문)
Files in This Item
There are no files associated with this item.
This item is cited by other documents in WoS
⊙ Detail Information in WoSⓡ Click to see webofscience_button
⊙ Cited 4 items in WoS Click to see citing articles in records_button

qr_code

  • mendeley

    citeulike


rss_1.0 rss_2.0 atom_1.0