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 divided 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-kappa B in RASMCs was immunocytochemically observed. Our results showed that MTT metabolism in RASMCs in the basic and AngII stimulated situation was inhibited by astilbin, and the cells numbers of G(0)/G(1) phase were increased and that of G(2)/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-kappa B 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 transition of RASMCs from G(0)/G(1) phase to S phase and by down-regulating the expression of NF-kappa B, c-myc gene.