目的:研究补阳还五汤诱导脑缺血后血管生成对侧脑室下区神经母细胞迁移的影响及机制。方法:采用线栓法诱导小鼠大脑中动脉阻塞模型,缺血30 min,分假手术组、模型组、补阳还五汤组和内皮抑素组。补阳还五汤组缺血后24 h开始灌胃补阳还五汤(20 g·kg-1),内皮抑素组在灌胃补阳还五汤同时皮下注射内皮抑素(10μg/只),每天1次,连续14 d。缺血后第14天,采用免疫荧光法检测缺血周边区微血管密度和神经母细胞数量,采用实时荧光定量PCR和Western blot检测基质细胞衍生因子1(stromal cell-derived factor-1,SDF-1)、脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)mRNA和蛋白表达。结果:与模型组比较,补阳还五汤组缺血周边区微血管密度和神经母细胞数量显著增多(P<0.01),SDF-1和BDNF mRNA和蛋白表达增加(P<0.01);与补阳还五汤组比较,内皮抑素组小鼠缺血周边区微血管密度和神经母细胞数量显著减少(P<0.01),SDF-1和BDNF mRNA和蛋白表达显著下降(P<0.01)。结论:补阳还五汤促进脑缺血后血管生成有助于侧脑室下区神经母细胞向缺血周边区迁移,机制可能与上调SDF-1和BDNF表达有关。 Objective: To investigate the effect of Buyang Huanwu Decoction induced angiogenesis on the migration of neuroblasts in the subventricular zone and its mechanism. Methods: The model of middle cerebral artery occlusion was induced by the method of thread plug. The rats were divided into three groups: sham operation group, model group, Buyang Huanwu Decoction group and endostatin group. Buyang Huanwu Decoction (20 g · kg -1) was administered 24 h after ischemia in Buyang Huanwu Decoction group. Endostatin (10 μg / Hg ), Once daily for 14 days. Fourteen days after ischemia, the number of microvessel density and neuroblasts in the peripheral area of ​​ischemic area were detected by immunofluorescence. The expression of stromal cell-derived factor-1 (SDF-1) was detected by real-time fluorescence quantitative PCR and Western blot. ), Brain-derived neurotrophic factor (BDNF) mRNA and protein expression. Results: Compared with the model group, the microvessel density and the number of neuroblasts in the peripheral area of ​​BYHWD group were significantly increased (P <0.01), the expressions of SDF-1 and BDNF mRNA and protein were increased (P <0.01) (P <0.01). The mRNA and protein expressions of SDF-1 and BDNF were significantly decreased in endostatin-treated mice (P <0.01). CONCLUSION: Buyang Huanwu Decoction can promote angiogenesis after cerebral ischemia and promote the migration of neuroblasts in the subventricular zone to the peripheral region. The mechanism may be related to up-regulating the expression of SDF-1 and BDNF.