Salvianolic acid B inhibits SDF-1α-stimulated cell proliferation and migration of vascular smooth muscle cells by suppressing CXCR4 receptor

Chun Hsu Pan, Ching Wen Chen, Ming Jyh Sheu, Chieh Hsi Wu

Research output: Contribution to journalArticlepeer-review

30 Citations (Scopus)

Abstract

Salvianolic acid B (Sal B), a bioactive compound from Salvia miltiorrhiza, widely used to treat cardiovascular diseases, and stromal cell-derived factor-1α (SDF-1α)/CXCR4 pathway has been correlated with balloon angioplasty-induced neointimal formation. The purposes of the present study were to investigate whether Sal B can inhibit SDF-1α/CXCR4-mediated effects on the cell proliferation and migration of vascular smooth muscle cells (VSMCs) and to examine its possible molecular mechanisms. Under 0.5% FBS medium, all of the cellular studies were investigated on VSMCs (A10 cells) stimulated with 10. ng/ml SDF-1α alone or co-treated with 0.075. mg/ml Sal B. Our results showed that SDF-1α markedly stimulated the cell growth and migration of A10 cells, whose effects can be significantly reversed by co-incubation of Sal B. Similarly, Sal B also obviously down-regulated the SDF-1α-stimulated up-regulation of CXCR4 (total and cell-surface levels), Raf-1, MEK, ERK1/2, phospho-ERK1/2, FAK and phospho-FAK as well as an increase of the promoter activity of NF-κB. Besides, Sal B also effectively attenuated balloon angioplasty-induced neointimal hyperplasia. In conclusion, suppressing the expression levels of CXCR4 receptor and downstream molecules of SDF-1α/CXCR4 axis could possibly explain one of the pharmacological mechanisms of Sal B on prevention of cell proliferation, migration and subsequently neointimal hyperplasia.

Original languageEnglish
Pages (from-to)98-105
Number of pages8
JournalVascular Pharmacology
Volume56
Issue number1-2
DOIs
Publication statusPublished - Jan 2012
Externally publishedYes

Keywords

  • Salvianolic acid B
  • Stromal cell-derived factor-1α
  • Vascular smooth muscle cells

ASJC Scopus subject areas

  • Molecular Medicine
  • Physiology
  • Pharmacology

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