Premium
Salvianolic acid B Inhibits Stromal Cell‐Derived Factor‐1/CXCR4 Axis and Promotes Apoptosis on Vascular Smooth Muscle Cells
Author(s) -
Wu ChiehHsi,
Pan ChuingHsu
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.603.3
Subject(s) - apoptosis , vascular smooth muscle , chemistry , stromal cell , flow cytometry , mapk/erk pathway , cell growth , microbiology and biotechnology , mtt assay , cell cycle , signal transduction , biology , cancer research , biochemistry , endocrinology , smooth muscle
We attempt to explore whether salvianolic acid B (Sal.B) can inhibit SDF‐1α‐induced biological effects on vascular smooth muscle cells (VSMCs). Cellular effects of Sal.B on cell proliferation and migration were investigated in A10 cells by MTT assay, wound‐healing assay and flow cytometry. The regulation of ERK‐MAPK pathway, apoptosis‐associated proteins, FAK, CXCR4 and SDF‐1α were determined. The apoptotic effect of Sal.B was also examined by DNA ladder assay and cell cycle analysis on cultured VSMCs. Furthermore, the luciferase‐based assay was used to measure the promoter activity of NF‐κB on cultured VSMCs stimulated by 10 ng.mL −1 SDF‐1α and/or 0.075 mg.mL −1 Sal.B. SDF‐1α stimulated cell proliferation and migration, which can be significantly inhibited by Sal.B. The up‐regulation of CXCR4, FAK, phosphor‐FAK, Raf‐1, MEK, ERK1/2 and phospho‐ERK1/2 induced by SDF‐1α was also markedly decreased by Sal.B. Additionally, Sal.B markedly increased Bcl‐2 but decreased caspase‐3 leading to apoptosis in a dose‐dependent manner. SDF‐1α‐mediated increase of NF‐κB promoter activity was suppressed by Sal.B treatment. The inhibitory and apoptotic effects of Sal.B on SDF‐1α‐triggered proliferation and migration of VSMCs were exerted through decreasing CXCR4 expression and its downstream pathways, and activating caspase‐dependent apoptosis pathway.