树鼩血栓性脑缺血时单胺氧化酶活性的变化及银杏内酯B作用机制探讨

目的:揭示血栓性脑缺血时缺血区和血清单胺氧化酶(MAO)活性变化及对血小板活化因子(PAF)受体拮抗剂银杏内酯B(GB)作用机理的探讨。方法:建立光化学诱导树鼠句血栓性脑缺血模型,用酶比色法测量缺血后4、24及72h中心区、半暗区、对侧区及血清的MAO活性,并用双缩脲法测定上述各区的蛋白含量。结果:脑缺血后不同时间缺血中心区MAO活性显著低于假手术组或对侧区,以72h最为明显;此时缺血半暗区和血清MAO活性明显高于假手术组(P＜0.01)。光化学反应后6h舌下静脉一次注射PAF受体拮抗剂GB(5mg·kg^-1)后24h时,半暗区MAO活性明显低于缺血组,而中心区则高于缺血组(P＜0.01)。MAO活性变化与相应区域蛋白含量改变一致(r=0.81,P＜0.05)。结论:脑缺血后中心区、半暗区MAO活性改变是相应区域单胺类递质消长变化的主要原因,MAO活性变化与神经元蛋白质合成能力的改变有关;GB的脑保护作用与其拮抗PAF受体和调节MAO活性而促进递质平衡有关。

Changes in monoamine oxidase activity during thrombotic cerebral ischemia and protection mechanisms of ginkgolide B in tree shrews

AIM:The present study was designed to examine changes in monoamine oxidase (MAO) activity during cerebral ischemia and whether ginkgolide B's brain protection challenges with inhibiting monoamine oxidase. METHODS: The focal thrombotic cerebral ischemia was formed by photochemistry-induced in tree shews.MAO activities in different areas which include ischemic,core, penumbra and contralater and serum, were tested by enzyme color-compared way. The protein contents in different area above was examined by amino acid autoanalytic apparatus. RESULTS:MAO activities in ischemic core in different group were much lower than that in the sham operation group and contralatetral areas, with its peak at seventy-two hours after occlusion, but that in penumbra and serum ascended. There were significant differences in MAO activities between ischemic group and control (P＜0.01). In ginkgolide B(GB) group, the MAO activities in all areas but not in core descended, significant differences(P＜0.01) between in GB group and in twenty-four hours after occlusion. Changes in MAO activity was consistent with alterations of brain proein content(r=0.81,P＜0.05). CONCLUSION:The changes in monoamine neurotransmitters in core and penumbra considerably depend on the alterations of MAO activities after thrombotically cerebral ischemia. Probably, protective effects of GB on ischemic neurons is related to its acting as antagonist of platelet activating factor and regulator of monoamine oxidase.