※ 引述《flysenta (senta)》之铭言： 让各位误会我想坐享其成真不好好意思，这是我大概翻译的结果，但是很多地方我 自己都觉得很奇怪，错误很多不太好意思PO上来，希望大家见谅。 为了澄清血管NADPH oxidase在蜘蛛网膜下腔出血後并发脑血管经孪的角色， 两者NADPH oxidase的活性或活化机制在脑血管和氧化?抑制蜘蛛膜下腔出血引发 脑血股经孪的评估。 中脑动脉管腔周围的改变在蜘蛛膜下腔出血後引发脑血管经孪 藉由2只出血的老鼠模型来做组织学测试。 NADPH oxidase的活性在脑血管中，以冷光试验在不同时间，间隔12小时到14天 注射自体血液至小脑延髓池後作测试。利用西方墨点法分析P47phox膜易位和 NADPH oxidase(gp91phox and p22phox)膜亚单位的蛋白质的表现。 中脑动脉管腔周围在第2次注射血液後，第一天开始下降，第五天达高峰， NADPH oxidase抑制剂diphenyleneiodonium 治疗有明显改善。24小时後第2次 注射的血液，两者血管皆产生超氧阴离子且NADPH oxidase活性明显的增加 P47phox膜易位,但是48小时酵素的活性重新回到正常值，无论如何， 透过这个实验观察到gp91phox和p22phox的改变是没有意义的。 这些发现解释NADPH oxidase活性在早期蜘蛛膜下腔出血，透过氧化玫成分的 扩大聚集，也许会使蜘蛛膜下腔出血的老鼠延迟经孪。 : 想麻烦帮我翻译这篇摘要，我已经看过大概知道意思，但是要完整翻译我翻不出中文， : 想请各位帮我翻译出完整的中文， 非常感谢!! : Background and Purpose–To clarify the role of vascular NAD(P)H oxidase in the : pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH), : both the activity and/or activation mechanisms of NAD(P)H oxidase in the : cerebral vasculature and the effect of oxidase inhibition on SAH-induced : cerebral vasospasm were assessed. : Methods—The changes in the luminal perimeter of the middle cerebral artery : were measured histologically after SAH was induced according to a 2-hemorrhage : model in rats. The NAD(P)H oxidase activity in the cerebral vasculature was : measured with a lucigenin assay at different time intervals from 12 hours to 14 : days after injection of autologous blood into cisterna magna. The membrane : translocation of p47phox and the protein expression of membrane subunits : (gp91phox and p22phox) of NAD(P)H oxidase were analyzed using Western blot : analysis. : Results—The luminal perimeter of the middle cerebral artery started to : decrease on day 1 and peaked on day 5 after a second injection of blood, : and these changes were significantly ameliorated by treatment with an NAD(P)H : oxidase inhibitor, diphenyleneiodonium. At 24 hours after the second injection : of blood, both vascular production of superoxide anion and NAD(P)H oxidase : activity were markedly increased with enhanced membrane translocation of : p47phox,but by 48 hours the enzyme activity had regained normal values. : However, no significant changes in the expression of : gp91phox and p22phox were observed throughout the experiments. : Conclusions—These findings suggest that the activation of NAD(P)H oxidase : through enhanced assembly of the oxidasecomponents in the early stages of : SAH might contribute to the delayed cerebral vasospasm in SAH rats. --

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