Ginsenoside Rh2 induces ligand-independent Fas activation via lipid raft disruption

Jae Sung Yi, Hyo Jung Choo, Bong Rae Cho, Hwan Myung Kim, Yong Nyun Kim, Young Mi Ham, Young Gyu Ko

Research output: Contribution to journalArticlepeer-review

52 Citations (Scopus)


Lipid rafts are plasma membrane platforms mediating signal transduction pathways for cellular proliferation, differentiation and apoptosis. Here, we show that membrane fluidity was increased in HeLa cells following treatment with ginsenoside Rh2 (Rh2), as determined by cell staining with carboxy-laurdan (C-laurdan), a two-photon dye designed for measuring membrane hydrophobicity. In the presence of Rh2, caveolin-1 appeared in non-raft fractions after sucrose gradient ultracentrifugation. In addition, caveolin-1 and GM1, lipid raft landmarkers, were internalized within cells after exposure to Rh2, indicating that Rh2 might disrupt lipid rafts. Since cholesterol overloading, which fortifies lipid rafts, prevented an increase in Rh2-induced membrane fluidity, caveolin-1 internalization and apoptosis, lipid rafts appear to be essential for Rh2-induced apoptosis. Moreover, Rh2-induced Fas oligomerization was abolished following cholesterol overloading, and Rh2-induced apoptosis was inhibited following treatment with siRNA for Fas. This result suggests that Rh2 is a novel lipid raft disruptor leading to Fas oligomerization and apoptosis.

Original languageEnglish
Pages (from-to)154-159
Number of pages6
JournalBiochemical and biophysical research communications
Issue number2
Publication statusPublished - 2009 Jul 24


  • Apoptosis
  • Fas activation
  • Ginsenoside Rh2
  • Lipid rafts

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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