Aim:To investigate the proliferation of vascular smooth muscle cells(VSMC)affected by ginsenoside Rg1 and further explore the molecular mechanism ofginsenoside Rg1 using proteomics.Methods:The proliferation of VSMC wasmeasured by MTS assay kit and flow cytometry.Proteomic alterations were ana-lyzed 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 fac-tor-α(TNF-α)treatment,and ginsenoside Rg1 treatment inhibited proliferation ina dose-dependent manner.Proteomic analysis showed 24 protein spots werechanged,including 17 spots that were increased and 7 spots that were decreased.Ginsenoside Rg1 could restore the expression levels of these proteins,at leastpartly,to basic levels of untreated cells.The expression of G-protein coupledreceptor kinase,protein kinase C(PKC)-ζ,N-ras protein were decreased,whilecycle related protein p21 was increased by ginsenoside Rgl in TNF-α treatedVSMC.Conclusion:PKC-ζ and p21 pathway might be the mechanism for inhibi-tory effects of ginsenoside Rg1 on proliferation of VSMC. Aim: To investigate the proliferation of vascular smooth muscle cells (VSMC) affected by ginsenoside Rg1 and further explore the molecular mechanism ofginsenoside Rg1 using proteomics. Methods: The proliferation of VSMC wasmeasured by MTS assay kit and flow cytometry. Proteomic alterations were ana-lyzed Using two-dimensional electrophoresis and peptide mass fingerprinting.Differential proteins found in proteomics were confirmed by RT-PCR.Results:The proliferation of VSMC was significantly significant after tumor necrosis fac-tor-α(TNF-α)treatment,and ginsenoside Rg1 treatment Suppressed proliferation ina dose-dependent manner. Proteomic analysis showed 24 protein spots werechanged, including 17 spots that were increased and 7 spots that were decreased.Ginsenoside Rg1 could restore the expression levels of these proteins, at leastpartly,to basic levels of untreated cells. The expression of G-protein coupled receptor kinase, protein kinase C(PKC)-ζ, N-ras protein were decreased, whilecycle related pro Tein p21 was increased by ginsenoside Rgl in TNF-α treated VSMC.Conclusion:PKC-ζ and p21 pathway might be the mechanism for inhibi-tory effects of ginsenoside Rg1 on proliferation of VSMC.