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Cardiovascular Pharmacology

Ginsenoside Rg1 inhibits proliferation of vascular smooth muscle cells stimulated by tumor necrosis factor-α

Abstract

Aim:

To investigate the proliferation of vascular smooth muscle cells (VSMC) affected by ginsenoside Rg1 and further explore the molecular mechanism of ginsenoside Rg1 using proteomics.

Methods:

The proliferation of VSMC was measured by MTS assay kit and flow cytometry. Proteomic alterations were analyzed using two-dimensional electrophoresis and peptide mass fingerprinting. Differential proteins found in proteomics were confirmed by RT-PCR.

Results:

The proliferation of VSMC was enhanced significantly after tumor necrosis factor-α (TNF-α) treatment, and ginsenoside Rg1 treatment inhibited proliferation in a dose-dependent manner. Proteomic analysis showed 24 protein spots were changed, including 17 spots that were increased and 7 spots that were decreased. Ginsenoside Rg1 could restore the expression levels of these proteins, at least partly, to basic levels of untreated cells. The expression of G-protein coupled receptor kinase, protein kinase C (PKC)-ζ, N-ras protein were decreased, while cycle related protein p21 was increased by ginsenoside Rg1 in TNF-α treated VSMC.

Conclusion:

PKC-ζ and p21 pathway might be the mechanism for inhibitory effects of ginsenoside Rg1 on proliferation of VSMC.

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Correspondence to Zeng-chun Ma or Yue Gao.

Additional information

Project supported by National Natural Sciences Foundation of China (The basic research of traditional Chinese medicine on genomics and proteomics, No 30271617)

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Ma, Zc., Gao, Y., Wang, Yg. et al. Ginsenoside Rg1 inhibits proliferation of vascular smooth muscle cells stimulated by tumor necrosis factor-α. Acta Pharmacol Sin 27, 1000–1006 (2006). https://doi.org/10.1111/j.1745-7254.2006.00331.x

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Keywords

  • cell cycle
  • ginsenoside Rg1
  • proteomics
  • tumor necrosis factor-α
  • vascular smooth muscle cells

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