title: Ginsenoside Rg1 inhibits proliferation of vascular smooth muscle cells stimulated by tumor necrosis factor-alpha.
abstract: OBJECTIVE
  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-alpha (TNF-alpha) 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)-zeta, N-ras protein were decreased, while cycle related protein p21 was increased by ginsenoside Rg1 in TNF-alpha treated VSMC.
  
  
  CONCLUSIONS
  PKC-zeta and p21 pathway might be the mechanism for inhibitory effects of ginsenoside Rg1 on proliferation of VSMC.
authors.affiliation: Institute of Radiation Medicine Sciences, Academy of Military Medical Sciences, Beijing 100850, China.
authors.forename: Zeng-Chun
authors.initials: ZC
authors.lastname: Ma
authors.forename: Yue
authors.initials: Y
authors.lastname: Gao
authors.forename: Yu-Guang
authors.initials: YG
authors.lastname: Wang
authors.forename: Hong-Ling
authors.initials: HL
authors.lastname: Tan
authors.forename: Cheng-Rong
authors.initials: CR
authors.lastname: Xiao
authors.forename: Sheng-Qi
authors.initials: SQ
authors.lastname: Wang
mesh_terms: D000818:Animals; D001011:Aorta / Q000166:cytology; D049109:Cell Proliferation / Q000187:drug effects*; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004365:Drugs, Chinese Herbal / Q000008:administration & dosage / Q000302:isolation & purification / Q000494:pharmacology; D016193:G1 Phase / Q000187:drug effects; D036145:Ginsenosides / Q000008:administration & dosage / Q000302:isolation & purification / Q000494:pharmacology*; D008297:Male; D032389:Myocytes, Smooth Muscle / Q000166:cytology / Q000378:metabolism*; D005894:Panax / Q000737:chemistry; D010946:Plants, Medicinal / Q000737:chemistry; D011493:Protein Kinase C / Q000378:metabolism; D016283:Proto-Oncogene Proteins p21(ras) / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*; D000099221:Protein Kinase C zeta
chemical_list: D004365:Drugs, Chinese Herbal; D036145:Ginsenosides; D011493:Protein Kinase C; D016283:Proto-Oncogene Proteins p21(ras); D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D000099221:Protein Kinase C zeta; C035054:ginsenoside Rg1