Morooka H, Hirotsune N, Wani T, Ohmoto T
Department of Neurological Surgery, Bizen City Hospital, Okayama, Japan.
Acta Neurochir Suppl (Wien). 1994;60:307-9. doi: 10.1007/978-3-7091-9334-1_82.
A new histofluorescence method by HPAA (p-hydroxyphenyl acetic acid) for free radicals in the brain tissue was devised to study neuronal damage induced by ischemia. Cerebral ischemia was produced in rats by injection of plastic microspheres and arachidonic acid (AA) into the right carotid artery. The concentration of malondialdehyde (MDA; free radical) in cerebral cortex of aminotriazol (an H2O2-dependent inhibitor of catalase) treated rats 2 h after stroke was 6.33 times the level before infarction, while the concentration of MDA in h-r SOD (free radical-scavenging enzyme) treated rats 2 h after stroke was significantly lower than in untreated rats. The histochemical findings demonstrated marked H2O2 production around blood vessels occluded by microspheres in the cerebral cortex of the aminotriazole treated rats 2 h after stroke together with disruption of the BBB. Light microscopical findings demonstrated extensive edematous changes in the aminotriazole treated rats 2 h after stroke, while pathological damage in SOD treated rat brains was absent or minimal. We conclude that free radicals are formed during ischemia, and that AA appears to be a major source of activated oxygen radicals. The findings indicate that SOD is protective against ischemia-induced neuronal damage.
设计了一种用对羟基苯乙酸（HPAA）检测脑组织中自由基的新组织荧光法，以研究缺血诱导的神经元损伤。通过向大鼠右颈动脉注射塑料微球和花生四烯酸（AA）来制造脑缺血。中风后2小时，用氨基三唑（一种过氧化氢依赖性过氧化氢酶抑制剂）处理的大鼠大脑皮层中丙二醛（MDA，自由基）的浓度是梗死前水平的6.33倍，而用h-r SOD（自由基清除酶）处理的大鼠中风后2小时MDA的浓度显著低于未处理的大鼠。组织化学结果表明，中风后2小时，氨基三唑处理的大鼠大脑皮层中被微球阻塞的血管周围有大量过氧化氢产生，同时血脑屏障遭到破坏。光学显微镜检查结果显示，中风后2小时，氨基三唑处理的大鼠出现广泛的水肿变化，而SOD处理的大鼠脑内病理损伤不存在或很轻微。我们得出结论，缺血期间会形成自由基，而且AA似乎是活性氧自由基的主要来源。研究结果表明，SOD对缺血诱导的神经元损伤具有保护作用。
