丁苯酞胶囊抗缺血脑损伤保护作用机制研究

目的：探讨丁苯酞胶囊抗缺血脑损伤保护的作用机制，探明其治疗VD的机制，为临床治疗VD提供理论依据。方法：采用双侧颈内动脉结扎（2-VO）法制作大鼠脑缺血再灌注VD模型，将丁苯酞胶囊分别以20、40、80mg／kg的剂量灌胃模型大鼠30天，用酶联免疫法测定大鼠大脑海马Ach、AchE、大脑皮层5-HT、NE、DA含量及血清ET、TXB2、6-Keto—PGFlα含量；用毛细管电泳法测定大鼠海马氨基酸Glu、Gly、Asp、GABA含量；用血液流变仪测定大鼠血液流变学参数，研究丁苯酞胶囊治疗VD的作用机制。结果：丁苯酞胶囊能增加海马中Ach含量和降低异常升高的AchE活性，各剂量均能明显增加大鼠海马氨基酸Glu、Asp、GABA的含量，且低剂量能明显增加Gly含量，对大脑皮层5-HT、DA水平有升高作用。此外，其还能显著改善缺血再灌注血管性痴呆大鼠的血液流变学参数，升高舒血管活性物质CGRP、6-Keto—PGF1α水平而降低缩血管活性物质TXB：的含量。结论：丁苯酞胶囊对治疗VD有显著作用，其机理与升高海马Ach含量和降低AchE活性、调节海马氨基酸含量和大脑皮层神经递质、改善血液流变性和调节血管活性物质有关。

Study on Pathogenesis for DI-3-n- butylphthalide Protection Against Ischemic Brain Injury

Objective： To understand the pathogenesis of vascular dementia. Methods： Using classic animal models to detect these dysmnesia. Adopting bilateral cervical arteries ligation on rats to make the animal model of cerebral ischemia and reperfusion and fill rats stomach with liquid medicine of dl-3-n- butylphthalide （NBP） as 20.40.80mg/kg for a month. Then detecting the purity of Ach, AchE, GABA, Glu, Gly, Asp in hippocampus; 5-HT, NE, DA in pallium and ET, TXB2, 6-Keto-PGFla, CGRP in serum of rats. Results： NBP have increased the purity of Ach, GABA, Glu, Asp in hippocampus and 5-HT, NE, DA in pallium and low- ered the activity of AchE; besides, it had significantly lowered ET, TXB2, 6-Keto-PGFla, CGRP in serum of rats. Conclusion： NBP could preferably play the role to treat dementia on account of its effect. The mechanism is probabely relevant to the purity of Ach in hippocampus, lowering the activity of AchE, adjusting the brain neurotransmitters and vascular active material, improving blood rheology and so on.