title: Effects of Panax notoginseng saponins on proliferation and apoptosis of vascular smooth muscle cells.
abstract: OBJECTIVE
  Atherosclerosis is a common cardiovascular disease, and linked with the development of many cardiovascular complications, such as myocardial ischemia and stroke. Although pathogenesis of atherosclerosis is not completely elucidated, increasing evidence has demonstrated that abnormal proliferation of vascular smooth muscle cells (VSMCs) plays an important role in formation of atherosclerosis. Previous studies showed that saponins from Panax notoginseng (PNS) possess anti-atherosclerotic properties. However, the mechanism of PNS against atherosclerosis is not well understood. Therefore, the present study observed the effects of PNS on proliferation and apoptosis of VSMCs.
  
  
  METHODS
  Rat VSMCs were cultured, and platelet-derived growth factor (PDGF) was used to stimulate cell proliferation. The viability of VSMCs was assessed with the MTT method. VSMCs apoptosis was detected by flow cytometry. Expressions of apoptosis related protein p53, Bax, caspase-3 and Bcl-2 were determined using Western blot.
  
  
  RESULTS
  Pretreatment of the cells with PNS (200, 400, 800 μg/mL) significantly inhibited proliferation of PDGF-stimulated VSMCs, and induced apoptosis of the proliferated VSMCs in a concentration-dependent way. Western blot analysis showed that PNS upregulated expressions of pro-apoptotic protein p53, Bax and caspase-3, downregulated expression of anti-apoptotic protein Bcl-2, and enlarged Bax/Bcl-2 ratio in the proliferated VSMCs induced by PDGF.
  
  
  CONCLUSIONS
  This study demonstrates that PNS both inhibits VSMCs proliferation and induces VSMCs apoptosis through upregulating p53, Bax, caspase-3 expressions and downregulating Bcl-2 expression, which constitute the pharmacological basis of its anti-atherosclerotic action.
authors.affiliation: Department of Pharmacology, Xi'an Jiaotong University School of Medicine, Xi'an 710061, China.
authors.forename: Li
authors.initials: L
authors.lastname: Xu
authors.forename: Jun-Tian
authors.initials: JT
authors.lastname: Liu
authors.forename: Na
authors.initials: N
authors.lastname: Liu
authors.forename: Pei-Pei
authors.initials: PP
authors.lastname: Lu
authors.forename: Xiao-Ming
authors.initials: XM
authors.lastname: Pang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D002317:Cardiovascular Agents / Q000302:isolation & purification / Q000494:pharmacology*; D053148:Caspase 3 / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D005434:Flow Cytometry; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D032389:Myocytes, Smooth Muscle / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D053723:Panax notoginseng / Q000737:chemistry; D010936:Plant Extracts / Q000302:isolation & purification / Q000494:pharmacology*; D010982:Platelet-Derived Growth Factor / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012503:Saponins / Q000302:isolation & purification / Q000494:pharmacology*; D013997:Time Factors; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D002317:Cardiovascular Agents; D010936:Plant Extracts; D010982:Platelet-Derived Growth Factor; D019253:Proto-Oncogene Proteins c-bcl-2; D012503:Saponins; D016159:Tumor Suppressor Protein p53; C505410:Casp3 protein, rat; D053148:Caspase 3