论文部分内容阅读
目的：探讨绞股蓝皂苷对脑干缺血性损伤的保护作用及其作用机制。方法：建立犬脑干缺血模型。在缺血前３ｈ，经十二指肠灌注给予绞股蓝皂苷０．１５ｇ·ｋｇ－１。观察脑干听觉诱发电位（ＢＡＥＰ）及病理（光镜及电镜）恢复率、磷脂酶Ａ２（ＰＬＡ２）和ＳＯＤ活性的动态变化。结果：在基底动脉夹闭后１，３，６及１２ｈ，绞股蓝皂苷组ＢＡＥＰ及病理恢复率逐渐升高，ＰＬＡ２活性逐渐降低（晚期突出），ＳＯＤ活性逐渐升高（早期明显），与缺血组比较，均有显著性差异（Ｐ＜０．０１）。结论：绞股蓝皂苷对犬脑干缺血有较好的保护作用，其机制可能与升高ＳＯＤ活性及降低ＰＬＡ２活性有关，早期以升高ＳＯＤ活性为主，晚期以降低ＰＬＡ２活性为主
Objective: To investigate the protective effect and mechanism of gypenosides on ischemic brainstem injury. METHODS: A canine model of brain stem ischemia was established. Three hours before ischemia, gypenoside 0.15 g·kg-1 was administered via duodenal infusion. The dynamic changes of brain stem auditory evoked potential (BAEP) and pathological (light and electron microscope) recovery rates, phospholipase A2 (PLA2) and SOD activity were observed. RESULTS: At 1, 3, 6 and 12 h after the occlusion of the basilar artery, the BAEP and the pathological recovery rate of the gypenoside group gradually increased, the PLA2 activity gradually decreased (later prominent), the SOD activity gradually increased (early obvious), and ischemia There was a significant difference between the groups (P<0.01). Conclusion: Gynostemma saponin has a good protective effect on brain stem ischemia in dogs, and its mechanism may be related to the increase of SOD activity and the decrease of PLA2 activity. In the early stage, SOD activity was mainly increased, and PLA2 activity was decreased in late stage.