Objective To observe the role and mechanism of miR-30b in apoptosis of vascular smooth muscle cells induced by high phosphorus. Methods VSMCs from the rat thoracic aorta were cultured in vitro and divided into a normal group and high phosphorus group stimulated by 10 mmol / L β-glycerophosphate. Expression of miR-30b in VSMCs was quantified by Real-time PCR, and expression of pro-apoptotic protein BAX and anti-apoptotic protein Bcl-2 was determined by Western blot. Cell proliferation was assessed by MTT assays, and apoptosis was detected by flow cytometry. To verify the effect of miR-30b on VSMCs apoptosis, inhibitor-30b and mimic-30b were applied to observe changes in proliferation and apoptosis of VSMCs and expression of BAX and Bcl-2. Results (1)The effect of high phosphorus on apoptosis of VSMCs: Flow cytometry showed that apoptosis cells of VSMCs in high phosphorus group increased significantly (P<0.05). The results of MTT showed that the proliferation of cells in high phosphorus group decreased ( P< 0.05). The expression of BAX increased and Bcl-2 decreased in high phosphorus group (P<0.05). The expression of miR-30b in high phosphorus group decreased significantly (P<0.05). (2) Effect of miR-30b on apoptosis of VSMCs: After transfection of inhibitor-30b, the number of apoptotic cells in VSMCs increased significantly (P<0.05). After transfection of inhibitor-30b, MTT assay showed that cell proliferation decreased (P<0.05). The expression of BAX increased and the expression of Bcl-2 decreased after transfection of inhibitor-30b (P<0.05). After mimic-30b transfection, the apoptotic cells of VSMCs decreased significantly (P<0.05). After transfection of mimic-30b, the expression of BAX decreased and the expression of Bcl-2 increased (P<0.05). Conclusions High phosphorus induces apoptosis. A possible mechanism is that high phosphorus inhibits miR-30b expression and then promotes expression of apoptosis gene BAX and decreases expression of anti-apoptosis gene Bcl-2, which leads to VSMCs apoptosis.