RGD Reference Report - Ginsenoside Rg1 inhibits vascular intimal hyperplasia in balloon-injured rat carotid artery by down-regulation of extracellular signal-regulated kinase 2. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

Ginsenoside Rg1 inhibits vascular intimal hyperplasia in balloon-injured rat carotid artery by down-regulation of extracellular signal-regulated kinase 2.

Authors: Gao, Yang  Deng, Jiang  Yu, Xue-Fang  Yang, Dan-Li  Gong, Qi-Hai  Huang, Xie-Nan 
Citation: Gao Y, etal., J Ethnopharmacol. 2011 Nov 18;138(2):472-8. doi: 10.1016/j.jep.2011.09.029. Epub 2011 Sep 22.
RGD ID: 401976490
Pubmed: PMID:21964194   (View Abstract at PubMed)
DOI: DOI:10.1016/j.jep.2011.09.029   (Journal Full-text)


ETHNOPHARMACOLOGICAL RELEVANCE: 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.
MATERIALS AND 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.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Intimal Hyperplasia treatmentISODusp1 (Rattus norvegicus)401976490; 401976490 RGD 
Intimal Hyperplasia treatmentIEP 401976490; 401976490 RGD 
Intimal Hyperplasia treatmentISOMapk1 (Rattus norvegicus)401976490; 401976490 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Dusp1  (dual specificity phosphatase 1)
Mapk1  (mitogen activated protein kinase 1)

Genes (Mus musculus)
Dusp1  (dual specificity phosphatase 1)
Mapk1  (mitogen-activated protein kinase 1)

Genes (Homo sapiens)
DUSP1  (dual specificity phosphatase 1)
MAPK1  (mitogen-activated protein kinase 1)


Additional Information