※ 引述《flysenta (senta)》之銘言： 讓各位誤會我想坐享其成真不好好意思，這是我大概翻譯的結果，但是很多地方我 自己都覺得很奇怪，錯誤很多不太好意思PO上來，希望大家見諒。 為了澄清血管NADPH oxidase在蜘蛛網膜下腔出血後併發腦血管經孿的角色， 兩者NADPH oxidase的活性或活化機制在腦血管和氧化?抑制蜘蛛膜下腔出血引發 腦血股經孿的評估。 中腦動脈管腔周圍的改變在蜘蛛膜下腔出血後引發腦血管經孿 藉由2隻出血的老鼠模型來做組織學測試。 NADPH oxidase的活性在腦血管中，以冷光試驗在不同時間，間隔12小時到14天 注射自體血液至小腦延髓池後作測試。利用西方墨點法分析P47phox膜易位和 NADPH oxidase(gp91phox and p22phox)膜亞單位的蛋白質的表現。 中腦動脈管腔周圍在第2次注射血液後，第一天開始下降，第五天達高峰， NADPH oxidase抑制劑diphenyleneiodonium 治療有明顯改善。24小時後第2次 注射的血液，兩者血管皆產生超氧陰離子且NADPH oxidase活性明顯的增加 P47phox膜易位,但是48小時酵素的活性重新回到正常值，無論如何， 透過這個實驗觀察到gp91phox和p22phox的改變是沒有意義的。 這些發現解釋NADPH oxidase活性在早期蜘蛛膜下腔出血，透過氧化玫成分的 擴大聚集，也許會使蜘蛛膜下腔出血的老鼠延遲經孿。 : 想麻煩幫我翻譯這篇摘要，我已經看過大概知道意思，但是要完整翻譯我翻不出中文， : 想請各位幫我翻譯出完整的中文， 非常感謝!! : 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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