Inhibitory effects and mechanism of tanshinone IIA on proliferation of rat aortic smooth muscle cells.
- Author:
Xin LI
1
;
Jun-rong DU
;
Bo BAI
;
Yan YU
;
Xiao-yuan ZHENG
;
Fang YANG
;
Hu ZHENG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Aorta; cytology; drug effects; Cell Cycle; drug effects; Cell Proliferation; drug effects; Cells, Cultured; Diterpenes, Abietane; Down-Regulation; Gene Expression; drug effects; Myocytes, Smooth Muscle; cytology; drug effects; Phenanthrenes; pharmacology; Proto-Oncogene Proteins c-fos; genetics; metabolism; Rats
- From: China Journal of Chinese Materia Medica 2008;33(17):2146-2150
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of tanshinone IIA (TA, one of the active components of Salvia miltiorrhiza Bge), on the proliferation of cultured rat vascular smooth muscle cells (VSMC), and to clarity the probable mechanism.
METHODCell culture technique was used in vitro and treated with or without 10% FBS. The inhibitory effect of TA on proliferation of VSMC was observed by cell count, MTU metabolism measuring and BrdU incorporation assay. Flow cytometry was performed to track cell cycle progression. Western bolts were performed to evaluate ERK1/2 activity. The expression of c-fos was examined by RT-PCR.
RESULTThe results of cell number, MTU assay and BrdU incorporation showed that TA cound significantly inhibit 10% FBS induced proliferation in a dose-dependent manner. Flow cytometry (FCM) analysis indicated that the G5/G1 phase fraction ratio of TA group was higher than that of 10% FBS group, while the S-phase fraction ratio was lower than that of 10% FBS group. Western blot's results displayed that TA inhibited the phosphorylation of ERK1/2, and in accordance with this findings. TA could decrease the early elevation of c-fos expression.
CONCLUSIONThese results suggest that TA can inhibit 10% FBS induced the proliferation of VSMC. This effect may be related to its blocking VSMCs cell cycle in G0/G1 phase, inhibiting of the ERK1/2 activity, and decreasing the expression of c-fos.