title: Ginsenoside Rg1 inhibits vascular intimal hyperplasia in balloon-injured rat carotid artery by down-regulation of extracellular signal-regulated kinase 2.
abstract: BACKGROUND
  Ginsenoside Rg1 (Rg1) is one of the main active components of Panax ginseng a well-known herbal medicine. It has been demonstrated to inhibit proliferation of vascular smooth muscle cells (VSMCs) induced by tumor necrosis factor-αin vitro. The present study is aimed to examine the possible effects of Rg1 on vascular neointimal hyperplasia in balloon-injured carotid artery of rats in vivo.
  
  
  METHODS
  The animal model was established by rubbing the endothelia with a balloon catheter in the common carotid artery (CCA) of male Sprague Dawley rats. Then the rats were intraperitoneally injected with distilled water in model group and sham operation control, or with Rg1 4, 8 and 16mg/kg/d in other balloon injured groups. After consecutive 14 days, the vascular intimal hyperplasia was evidenced by histopathological alterations of the CCA and by changes observed in the marker of the proliferation of VSMCs-the proliferating cell nuclear antigen (PCNA). The protein expressions of PCNA and the phosphorylated extracellular signal-regulated kinase2 (p-ERK2) as well as mitogen-ativated protein kinase phosphatase-1 (MKP-1) were examined by immunohistochemistry; while the expressions of proto-oncogene (c-fos), ERK2 and smooth muscle α-actin (SM α-actin) mRNA were analyzed by Real-Time RT-PCR.
  
  
  RESULTS
  Rg1 administration could significantly ameliorate the histopathology of CCA and decrease the protein expression of PCNA induced by endothelia rubbing; and Rg1 medication also significantly decreased the expressions of p-ERK2 protein, ERK2 and c-fos mRNA in vessel wall, but up-regulated the MKP-1 expression, which was reported to inactivate mitogen-ativated protein kinase pathway. Furthermore, Rg1 could elevate the decreased SM α-actin mRNA expression induced by balloon injury.
  
  
  CONCLUSIONS
  Rg1 can suppress the vascular neointimal hyperplasia induced by balloon injury, the mechanism may be involved in the inhibition on ERK2 signaling, and related, at least partly, to the increase in MKP-1 expression.
authors.affiliation: Department of Pharmacology and the Key Laboratory of Basic Pharmacology of Guizhou Province, Zunyi Medical College, No. 201 Dalian Road, Zunyi, Guizhou 563000, PR China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Gao
authors.forename: Jiang
authors.initials: J
authors.lastname: Deng
authors.forename: Xue-Fang
authors.initials: XF
authors.lastname: Yu
authors.forename: Dan-Li
authors.initials: DL
authors.lastname: Yang
authors.forename: Qi-Hai
authors.initials: QH
authors.lastname: Gong
authors.forename: Xie-Nan
authors.initials: XN
authors.lastname: Huang
mesh_terms: D000818:Animals; D001483:Base Sequence; D002339:Carotid Arteries / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D017931:DNA Primers; D015536:Down-Regulation; D036145:Ginsenosides / Q000494:pharmacology*; D006965:Hyperplasia; D007150:Immunohistochemistry; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism*; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017539:Tunica Intima / Q000187:drug effects* / Q000473:pathology
chemical_list: D017931:DNA Primers; D036145:Ginsenosides; D019950:Mitogen-Activated Protein Kinase 1; C035054:ginsenoside Rg1