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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.