College of Pharmacy and Institute of Material Medica, Binzhou Medical University, Yantai, China.
Basic Clin Pharmacol Toxicol. 2011 Jan;108(1):21-7. doi: 10.1111/j.1742-7843.2010.00620.x.
We investigated whether 8-O-acetyl shanzhiside methylester (ND01) regulates angiogenesis and thereby improves functional outcome after stroke. Adult male rats were subjected to 1 hr of middle cerebral artery occlusion (MCAO) and reperfusion, and treated with or without different doses (5 and 10 mg/kg) of ND01, starting 24 hr after ischaemia and reperfusion (I/R) and by intravenous injection daily for 14 days. Neurological functional tests were performed and cerebral Evans blue extravasation was measured. Angiogenesis and angiogenic factor expression were measured by immunohistochemistry and Western blot, respectively. The results indicated that ND01 significantly promoted angiogenesis in the ischaemic brain and improved functional outcome after stroke. ND01 also significantly increased vascularization compared with vehicle treatment. ND01 increased the expression of VEGF, Ang1, phosphorylation of Tie2 and Akt VEGF. The Ang1/Tie2 axis and Akt pathways appear to mediate ND01-induced angiogenesis.
我们研究了 8-O-乙酰山芝昔甲酯（ND01）是否通过调节血管生成从而改善中风后的功能预后。成年雄性大鼠进行 1 小时大脑中动脉闭塞（MCAO）和再灌注，并用或不用不同剂量（5 和 10mg/kg）的 ND01 治疗，从缺血再灌注（I/R）后 24 小时开始，并通过静脉注射每天 14 天。进行神经功能测试和脑 Evans 蓝渗出测量。通过免疫组织化学和 Western blot 分别测量血管生成和血管生成因子的表达。结果表明，ND01 可显著促进缺血性大脑中的血管生成，并改善中风后的功能预后。与载体处理相比，ND01 还显著增加了血管化。ND01 增加了 VEGF、Ang1、Tie2 磷酸化和 Akt VEGF 的表达。Ang1/Tie2 轴和 Akt 途径似乎介导了 ND01 诱导的血管生成。
