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Chem Biol Interact. 2018 Mar 1;283:75-83. doi: 10.1016/j.cbi.2018.02.002. Epub 2018 Feb 3.

Ginsenoside F1 suppresses astrocytic senescence-associated secretory phenotype.

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Intelligent Synthetic Biology Center, Daejeon 34141, Republic of Korea.
Intelligent Synthetic Biology Center, Daejeon 34141, Republic of Korea; Department of Biological Sciences, KAIST, Daejeon 34141, Republic of Korea. Electronic address:
Department of Food Science and Technology, College of Agriculture and Biotechnology, Chungnam National University, Daejon 305764, Republic of Korea.
Department of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Republic of Korea.


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-κB 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-κB inhibitor, BAY 11-7092, also suppressed the secretion of IL-6 and IL-8, suggesting NF-κB 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.


Astrocytic senescent; Ginsenoside F1; Glioblastoma; NF-κB; SASP; p38MAPK

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