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背景:冷冻所致脑水肿,被认为是一种典型的血管源性脑水肿。许多化学递质参与这一过程,其中氧自由基起主导作用,采用银杏叶提取物所具有的氧自由基清除剂作用,可望发挥抗脑水肿及脑保护作用。目的:探讨银杏叶提取物对冷冻所致兔脑水肿的保护作用及其机制。设计:采用完全随机设计,空白对照实验。地点和材料:同济医科大学附属同济医院神经外科,材料由同济医科大学动物中心提供。健康中国家兔30只,体重2.0～2.8kg,雌雄不拘.干预:30只健康中国家兔,单纯随机分为3组:对照组、脑水肿模型组、EGb761处理组,3组家兔分别在术后6,24h断头取脑测定脑组织含水量、脂质过氧化物含量及超氧化物歧化酶活性。主要观察指标:测定脑含水量,脑组织LPO含量及SOD活力的变化。结果:术后6h和24h,脑水肿模型组脑组织LPO含量犤(6.82±1.36)μmol/L,(7.95±2.12)μmol/L犦及脑组织含水量犤(78.56±0.61)%;(79.86±0.54)%犦呈进行性增高,SOD活性则呈进行性下降(P<0.05);EGb761处理组脑组织LPO含量及脑组织含水量增加不显著,且SOD活性回升(P<0.05)。结论:EGb761具有抗脑水肿和保护脑组织的作用。而其减轻脂质过氧化反应,保护脑组织内源性SOD活性,增强脑组织自身清除氧自由基的功能,则可能是其重要的药理作用机制之一。
BACKGROUND: Brain edema caused by freezing is considered to be a typical vasogenic brain edema. Many chemical transmitters participate in this process. Oxygen radicals play a major role. Using the oxygen free radical scavenger that Ginkgo biloba extract has, it is expected to exert anti-cerebral edema and brain protection. Objective: To investigate the protective effect of Ginkgo biloba extract on rabbit brain edema induced by freezing and its mechanism. Design: A completely random design, blank control experiment. Location and Materials: Department of Neurosurgery, Tongji Hospital, Tongji Medical University, provided by the Animal Center of Tongji Medical University. Thirty rabbits in a healthy country were weighed between 2.0 and 2.8 kg, male or female. Intervention: Thirty healthy Chinese rabbits were randomly divided into three groups: control group, cerebral edema model group, and EGb761 treatment group. The three groups of rabbits were After 6 and 24 hours of operation, the brain was removed and the brain tissue water content, lipid peroxide content and superoxide dismutase activity were measured. MAIN OUTCOME MEASURES: Changes in brain water content, brain tissue LPO content and SOD activity were determined. RESULTS: At 6h and 24h after operation, the LPO content in the cerebral edema model group was (6.82±1.36) μmol/L, (7.95±2.12) μmol/L and the brain tissue water content was (78.56±0.61)%; (79.86) There was a progressive increase in ± 0.54 % of sputum and SOD activity was progressively decreased (P <0.05). The EGb761 treatment group had no significant increase in LPO content and brain tissue water content, and SOD activity increased (P <0.05). Conclusion: EGb761 has anti-cerebral edema and protects brain tissue. The reduction of lipid peroxidation, the protection of endogenous SOD activity in brain tissue, and the enhancement of the function of brain tissue to scavenge oxygen free radicals may be one of its important pharmacological mechanisms.