Astilbin Inhibits Proliferation of Rat Aortic Smooth Muscle Cells Induced by Angiotensin Ⅱ and Down-regulates Expression of Protooncogene
10.1007/s11596-012-0032-8
- Author:
LI PING
1
;
GAO SIHAI
;
JIE WEI
;
AO QILIN
;
HUANG YAFEI
Author Information
1. Department of Cardiovascular Surgery,Union Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430022,China
- Keywords:
astilbin;
vascular smooth muscle cells;
proliferation;
angiotensin Ⅱ;
protooncogene;
NF-κB
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2012;32(2):181-185
- CountryChina
- Language:Chinese
-
Abstract:
This study examined the effect of astilbin on the proliferation of rat aortic smooth muscle cells (RASMCs) induced by angiotensin Ⅱ (Ang Ⅱ) and explored the possible mechanisms.Cell proliferation model of RASMCs was induced by treatmente with Ang Ⅱ.Cells were randomly divided to 8 groups.Normally cultured VSMCs serves as blank control group; in Ang Ⅱ model group,cells were treated with AngⅡ at 10-7 mol/L; in three astilbin groups,cells were treated with 10,15,30 mg/L of astilbin; in three Ang Ⅱ +astilbin groups,cells were treated with Ang Ⅱ (at 1 0-7 mol/L) and astilbin at 10,15,30 mg/L.Cell proliferation ability was detected by MTT method and the cell cycles and proliferation index were flow cytometrically determined.The expression of c-myc mRNA was assessed by using reverse transcription polymerase chain reaction (RT-PCR),and the expression of NF-κB in RASMCs was immunocytochemically observed.Our results showed that MTT metabolism in RASMCs in the basic and Angll stimulated situation was inhibited by astilbin,and the cells numbers of G0/G1 phase were increased and that of G2/S phase were decreased markedly.Not only highly expression of c-myc gene stimulated by Ang Ⅱ could be inhibited by Astilbin significantly,but also the expression of NF-κB protein can be down regulated by Astilbin.We are led to conclude that astilbin astilbin can inhibit the Ang Ⅱ -mediated proliferation of RASMCs by blocking the transition of RASMCs from Go/G1 phase to S phase and by down-regulating the expression of NF-κB,c-mvc gene.
