Astilbin Inhibits Proliferation of Rat Aortic Smooth Muscle Cells Induced by Angiotensin Ⅱ and Down-regulates Expression of Protooncogene

This study examined the effect of astilbin on the proliferation of rat aortic smooth muscle cells (RASMCs) induced by angiotensin Ⅱ (AngⅡ) and explored the possible mechanisms. Cell proliferation model of RASMCs was induced by treatmente with AngⅡ. Cells were randomly di-vided to 8 groups. Normally cultured VSMCs serves as blank control group; in AngⅡ 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 AngⅡ+astilbin groups, cells were treated with AngⅡ (at 10-7 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 metabo-lism in RASMCs in the basic and AngII 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 AngⅡ 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 AngⅡ-mediated proliferation of RASMCs by blocking the tran-sition of RASMCs from G0/G1 phase to S phase and by down-regulating the expression of NF-κB, c-myc gene.