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目的：研究骨形态发生蛋白-2（BMP-2）促进骨质疏松性成骨细胞成骨过程中血管内皮生长因子（VEGF）的作用机制。方法用最佳浓度的rhBMP-2干预成骨细胞，同时分别加入不同浓度的VEGF反义寡核苷酸（ASODNs）、苏拉明和外源性VEGF，继续培养48 h后检测碱性磷酸酶（ALP）活性，18 d后检测钙结节的形成。结果（1）大鼠全身骨密度：手术前后大鼠全身骨密度分别为（0.179±0.006）、（0.158±0.007）g/cm2，差异有统计学意义（t=4.180， P<0.05）。（2）VEGF ASODNs组和苏拉明组，其钙结节形成和ALP活性分别随其剂量增加而减少；添加外源性VEGF组，其钙结节形成和ALP活性不受其剂量大小影响。结论单独rhBMP-2能提高去卵巢骨质疏松大鼠骨髓间充质干细胞（BMSCs）的体外成骨能力，而VEGF则不行。VEGF在成骨细胞可能分泌某种物质，促进rhBMP-2诱导成骨活性。“,”Objective To study the mechanism of vascular endothelial growth factor(VEGF)in bone osteoporotic bone marrow stromal cells (BMSCs) induced bone morphogenetic by protein-2. Methods Optimal concentration protein-2 intervene osteoblasts,While add different concentration respectively VEGF antisense oligodeoxynucleotides(VEGF ASODNs), Suramin and exogenous VEGF. After 48 hours,observe the influence on alkaline phosphatase(ALP) activity .After 18 days,observe the influence on bone nodule formation of osteoblasts. Results ①Whole body bone mineral density of rats:the whole body bone mineral density of rats before and after operation were (0.179±0.007) g/cm2, (0.158 ± 0.006) g/cm2. Difference was statistically significant (t=4.180, P<0.05). ② The alkaline phosphatase(ALP) activity and bone nodule formation of osteoblasts reduce respectively With the increase of VEGF ASODNs and Suramin ,yet unaffect practically With the increase of exogenous VEGF. Conclusion Alonely RhBMP-2 can improve to ovary osteoporosis rat BMSCs in vitro osteogenesis ability, yet VEGF cannot. VEGF acts in an autocrine manner on the osteoblastic cells, at least partly in the process of osteogenesis induced by rhBMP-2.