绞股蓝皂苷脑干缺血性损伤保护作用及机制探讨

 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

The protective effect of gypenoside on brainstem ischemia and its mechanism

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 A₂(PLA₂) 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 PLA₂activity 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 PLA₂activity induced by ischemia (P<0.01) and stimulate the activity of superoxide dismutase (SOD).