Inhibitory effects of 2,3,4',5-tetrahydroxystilbene-2-O-β-D-glucoside on angiotensin II-induced proliferation of vascular smooth muscle cells.
- Author:
Xiao-le XU
1
;
Yan-juan HUANG
;
Dan-yan LING
;
Wei ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II; pharmacology; Animals; Cell Cycle; drug effects; Cell Proliferation; drug effects; Extracellular Signal-Regulated MAP Kinases; metabolism; Glucosides; pharmacology; Intracellular Space; metabolism; Male; Mitogen-Activated Protein Kinase Kinases; metabolism; Muscle, Smooth, Vascular; cytology; Myocytes, Smooth Muscle; cytology; drug effects; Phosphorylation; drug effects; Proliferating Cell Nuclear Antigen; metabolism; Proto-Oncogene Proteins; metabolism; RNA, Messenger; genetics; metabolism; Rats, Sprague-Dawley; Reactive Oxygen Species; metabolism; Stilbenes; pharmacology; Superoxide Dismutase; metabolism
- From: Chinese journal of integrative medicine 2015;21(3):204-210
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the effect of 2,3,4',5-tetrahydroxystilbene-2-O-β-D-glucoside (TSG), an active component extracted from the root of Polygonum multiflorum, on angiotensin II (Ang II)-induced proliferation of cultured rat vascular smooth muscle cells (VSMCs) and to identify the potential mechanism.
METHODSCell proliferation and cell cycle were determined by cell counting, 5-bromo-2'-deoxyuridine incorporation assay, proliferating cell nuclear antigen protein expression and flow cytometry. Levels of phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2), mitogenic extracellular kinase 1/2 (MEK1/2) and Src in VSMCs were measured by Western blot. The expression of c-fos, c-jun and c-myc mRNA were measured by reverse transcription polymerase chain reaction (RT-PCR). Intracellular reactive oxygen species (ROS) was measured by fluorescence assay.
RESULTSTSG significantly inhibited Ang II-induced VSMCs proliferation and arrested cells in the G /S checkpoint (P<0.05 or P<0.01). TSG decreased the levels of phosphorylated ERK1/2, MEK1/2 and Src in VSMCs (P<0.05 or P<0.01). TSG also suppressed c-fos, c-jun and c-myc mRNA expression <0.05 or P<0.01). In addition, the intracellular ROS was reduced by TSG (P<0.01).
CONCLUSIONSTSG inhibited Ang II-induced VSMCs proliferation. Its antiproliferative effect might be associated with down-regulation of intracellular ROS, followed by the suppression of the Src-MEK1/2-ERK1/2 signal pathway, and hence, blocking cell cycle progression.