绞股蓝皂苷脑干缺血性损伤保护作用及机制探讨  

The protective effect of gypenoside on brainstem ischemia and its mechanism

作　　者：李黔宁[1] 王东武[1] 岳桂明[1] 邓志宽[1] 何英[1] 杨红[1] 

机构地区：[1]第三军医大学新桥医院神经内科

出　　处：《中国药学杂志》1997年第8期466-469,共4页Chinese Pharmaceutical Journal

摘　　要：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。OBJECTIVE: To investigate the protective effect of gypenoside on brainstem ischemic injuries and its mechanism. METHODS: The model of brainstem ischemic injury in dogs was established by the occlusion of the basilar artery. Gypenoside (150 mg·kg -1 ) was intradudinally given at 3 h before occlusion. The changes of recovery rate of brainstem auditory evoked patenfials (BAEP) and pathology (observed under light and electron microscope), phospholipase A 2 (PLA 2) and SOD activity were observed. RESULTS: After 1, 3, 6, 12 hours occlusion of basilar artery, the recovery rate of BAEP and pathology increased, SOD activity elevated, while PLA 2 activity reduced in gypenoside treatment groups gradually, (P<0.01) compared with the ischemia groups. CONCLUSION: Gypenoside may have protective effects on brainstem ischemic injuries. Gypenoside may inhibit the activation of PLA 2 activity induced by ischemia (P<0.01) and stimulate the activity of superoxide dismutase (SOD).

关 键 词：脑干缺血 绞股蓝皂苷 绞股蓝 保护作用 

分 类 号：R285.5[医药卫生—中药学] R277.733.1[医药卫生—中医学]