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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-PGF1α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TXB2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。
OBJECTIVE: To investigate the mechanism of butylphthalide capsule in protecting against ischemic brain injury and to explore the mechanism of its treatment for VD, providing a theoretical basis for the clinical treatment of VD. Methods: VD model was established by bilateral carotid artery ligation (2-VO) in rats with cerebral ischemia-reperfusion. The rats were injected with butylphthalide 20, 80 and 80 mg / kg respectively for 30 days, Serum levels of ET, TXB2 and 6-Keto-PGF1α in hippocampal Ach and AchE, cerebral cortex were measured by enzyme-linked immunosorbent assay (ELISA). Contents of Glu and Gly in rat hippocampus were determined by capillary electrophoresis. Asp and GABA levels were measured. The hemorrheological parameters of rats were determined by hemorrheology and the mechanism of action of butylphthalide capsules on VD was studied. Results: Butylphthalide capsule could increase the content of Ach in hippocampus and decrease the abnormally elevated AchE activity. Each dose could significantly increase the content of Glu, Asp and GABA in hippocampus of rats, and the low dose could significantly increase the content of Gly. Cortical 5-HT, DA levels have increased role. In addition, it can significantly improve the blood rheology parameters of ischemia-reperfusion vascular dementia rats and increase the level of vasoactive substances CGRP, 6-Keto-PGF1α and reduce the content of TXB2 of vasoconstrictor. CONCLUSION: Butylphthalide capsule has a significant effect on the treatment of VD. Its mechanism is related to increasing Ach content and decreasing AchE activity in the hippocampus, regulating hippocampal amino acid content and neurotransmitter in the cerebral cortex, improving hemorrheology and regulating vasoactive substances.