染料木黄酮通过促进VEGF表达改善去势大鼠骨质疏松的作用机制

摘要

目的 观察染料木黄酮(Genistein Gen)通过促进VEGF表达改善去势大鼠骨质疏松的作用机制.方法 建立绝经大鼠模型,6月龄雌性大鼠40只,随机分为对照组,假手术组、去势组、Gen干预6周组、Gen干预12周组.光镜下观察各组股骨头结构,分析大鼠股骨头空缺骨陷窝数的变化.ELISA检测血管内皮生长因子(VEGF),观察VEGFmRNA原位杂交表达强度并分析.结果 与对照组相比,去势组骨密度值下降,Tb.Th明显下降(P＜0.05).干预10周组骨密度值明显升高,Tb.Th明显升高,差异均有统计学意义(P＜0.05).糖尿病大鼠股骨头随病程发展骨小梁变稀薄.Gen对去卵巢大鼠血清中VEGF的表达无影响.VEGF mRNA在骨髓腔血管内皮细胞表达上升(P＜0.05).结论 Gen可促进血管内皮细胞增殖,促进血管形成,改善去势大鼠骨质疏松抗骨质疏松倾向.%Objective To observe the mechanism of genistein (Gen) on osteoporosis in ovariectomized rats by promoting VEGF expression.Methods Forty 6-month-old female rats were randomly divided into control group,sham operation group,castration group,Gen intervention 6-week group,and Gen intervention 10-week group.Femoral head structure of each group was observed under light microscope.The changes of the number of vacancy lacunae in rat femoral head was analyzed.Vascular endothelial growth factor (VEGF) was detected with ELISA,and the expression intensity of VEGF mRNA in situ hybridization was observed and analyzed.Results Compared with that in the control group,bone mineral density and Tb.Th decreased significantly (P ＜ 0.05) in the castration group.Bone mineral density and Tb.Th increased significantly in the Gen intervention 10-week group,and the differences were statistically significant (P ＜ 0.05).The trabecular bone became thinner with the development of disease course in the diabetic rat femoral head.Gen had no effect on the expression of VEGF in serum of ovariectomized rats.The expression of VEGF mRNA in bone marrow-derived vascular endothelial cells increased (P ＜ 0.05).Conclusion Gen promotes the proliferation of vascular endothelial cells,promotes angiogenesis,and improves the anti-osteoporosis tendency in ovariectomized rats.