Red Ginseng Attenuates the Hepatic Cellular Senescence in Aged Mice.
Da-Yeon LeeJuliana ArndtJennifer F O'ConnellJosephine M EganYoo KimPublished in: Biology (2024)
Cellular senescence is defined as an irreversible cell cycle arrest accompanied by morphological and physiological alterations during aging. Red ginseng (RG), processed from fresh ginseng ( Panax ginseng C.A. Meyer) with a one-time steaming and drying process, is a well-known beneficial herbal medicine showing antioxidant, anti-inflammatory, and anti-aging properties. The current study aimed to investigate the benefits of RG in alleviating hepatic cellular senescence and its adverse effects in 19-month-old aged mice. We applied two different intervention methods and durations to compare RG's effects in a time-dependent manner: (1) oral gavage injection for 4 weeks and (2) ad libitum intervention for 14 weeks. We observed that 4-week RG administration was exerted to maintain insulin homeostasis against developing age-associated insulin insensitivity and suppressed cellular senescence pathway in the liver and primary hepatocytes. Moreover, with remarkable improvement of insulin homeostasis, 14-week RG supplementation downregulated the activation of c-Jun N-terminal kinase (JNK) and its downstream transcriptional factor nuclear factor-κB (NF-κB) in aged mice. Lastly, RG treatment significantly reduced the senescence-associated β-galactosidase (SA-β-gal)-positive cells in primary hepatocytes and ionizing radiation (IR)-exposed mouse embryonic fibroblasts (MEFs). Taken together, we suggest that RG can be a promising candidate for a senolytic substance by preventing hepatic cellular senescence.
Keyphrases
- cell cycle arrest
- dna damage
- endothelial cells
- nuclear factor
- type diabetes
- stress induced
- cell death
- anti inflammatory
- randomized controlled trial
- induced apoptosis
- pi k akt
- signaling pathway
- high fat diet induced
- oxidative stress
- toll like receptor
- glycemic control
- gene expression
- lps induced
- clinical trial
- insulin resistance
- protein kinase
- skeletal muscle
- tyrosine kinase