[Effect of ginsenoside Rg1 on expression of p21, cyclin E and CDK2 in the process of cell senescence]

Chao-hui Zhao1, Xiao-chun Chen, Jian-sheng Jin

  • 1The Affiliated Union Hospital, Fujian Medical University, Fujian Institute of Geriatrics, Fuzhou 350001, China.

Abstract

Insights

Ginsenoside Rg1 protects WI-38 cells from oxidative stress-induced senescence by modulating p21, cyclin E, and cyclin-dependent kinase 2 (CDK2) levels. This suggests a key role for these proteins in Rg1

Area of Science:

  • Cell Biology
  • Pharmacology
  • Gerontology

Background:

  • Oxidative stress contributes to cellular senescence.
  • Ginsenoside Rg1 is a compound with potential protective properties.
  • Cellular senescence is implicated in aging and age-related diseases.

Purpose of the Study:

  • To investigate the protective effect of ginsenoside Rg1 against tert-butylhydroperoxide (t-BHP)-induced senescence in WI-38 cells.
  • To explore the involvement of p21, cyclin E, and cyclin-dependent kinase 2 (CDK2) in this protective mechanism.

Main Methods:

  • WI-38 cells were exposed to t-BHP to induce senescence.
  • Cellular senescence was assessed using assays for cellular ultrastructure, cytometric analysis, and beta-galactosidase staining.
  • Protein levels of p21, cyclin E, and CDK2 were quantified via Western blot.

Main Results:

  • Ginsenoside Rg1 pretreatment significantly reduced t-BHP-induced senescence in WI-38 cells.
  • Rg1 treatment decreased the protein level of p21.
  • Rg1 treatment increased the protein levels of cyclin E and CDK2.

Conclusions:

  • p21, cyclin E, and CDK2 are likely involved in the protective action of ginsenoside Rg1 against oxidative stress-induced senescence.
  • These findings highlight a potential therapeutic role for ginsenoside Rg1 in mitigating cellular senescence.

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