【摘要】 目的：从小窝蛋白1(Caveolin1)-血管内皮生长因子（VEGF）信号探讨补阳还五汤对脑缺血小鼠血管新生的影响。方法：将野生型（WT）和Caveolin1敲除（KO）小鼠随机分为模型组（WTM、KOM）和补阳还五汤组（WTB、KOB），每组12只，大脑中动脉闭塞法复制脑缺血模型，术后7、14 d检测小鼠神经功能情况，免疫组化检测血管性血友病因子（vWF）、VEGF及其受体（VEGFR2）表达，RT-qPCR检测VEGF、VEGFR2 mRNA表达。结果：Caveolin1敲除可加重脑缺血小鼠神经功能缺损，抑制血管新生，7、14 d与WTM比较差异有统计学意义（P<0.05）；补阳还五汤治疗可减轻WTM和KOM小鼠神经功能缺损、增加血管新生，差异有统计学意义（P<0.05）。Caveolin1敲除可减少VEGF与VEGFR2阳性细胞数和mRNA表达，7、14 d与WTM比较差异有统计学意义（P<0.05）；补阳还五汤可增加VEGF与VEGFR2阳性细胞数和mRNA表达，WTB与WTM、KOB与KOM之间比较差异有统计学意义（P<0.05）。结论：Caveolin1通过VEGF信号调控脑缺血后血管新生，该通路可能是补阳还五汤抗脑缺血损伤的机制之一。更多还原

【Abstract】 Objective: To study the effects of Buyang Huanwu Decoction on angiogenesis in mice with cerebral ischemia via Caveolin1-VEGF signal. Methods: Healthy adult wild type(WT) and homologous Caveolin1 knockout(KO) mice were randomly divided into model group(WTM and KOM), BYHWD group(WTB and KOB), 12 rats in each group. Cerebral ischemia model was induced by MCAO. At 7,14 d, the neurologic function was evaluated, von Willebrand Factor(vWF) and the expression of VEGF and VEGFR2 were detected by immunohistochemistry, VEGF and VEGFR2 mRNA were detected by RT-qPCR. Results: Caveolin1 knockout aggravated the neurological deficit and inhibited angiogenesis in MCAO mice, and the difference was significant compared with WTM at 7, 14 days(P<0.05); Buyang Huanwu Decoction alleviated neurological deficit and increased angiogenesis in WT and KO mice, and there was significant difference compared with the group before BYHWD treatment(P<0.05). Caveolin1 knockout reduced the number of VEGF and VEGFR2-positive cells and levels of mRNA, there were significant difference at 7, 14 days compared with WTM respectively(P<0.05); Buyang Huanwu Decoction increased the number of VEGF and VEGFR2-positive cells and levels of mRNA. There was significant difference between WTB, KOM and KOB(P<0.05). Conclusion: Caveolin1 regulates angiogenesis after cerebral ischemia through VEGF signal, which may be another mechanism of Buyang Huanwu Decoction antagonized ischemia injury.更多还原