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題 名 | Nitric Oxide Scavenger Carboxy-PTIO Reduces Infarct Volume Following Permanent Focal Ischemia=一氧化氮補捉物Carboxy-PTIO降低永久性腦梗塞的神經保護作用--初步報告 |
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作 者 | 方詩元; 曾稼志; 楊曜臨; 李宜堅; 陳鴻儀; 陳宗鷹; | 書刊名 | 麻醉學雜誌 |
卷 期 | 44:3 民95.09 |
頁 次 | 頁141-146 |
分類號 | 416.5 |
關鍵詞 | 腦缺血; 一氧化氮; 自由基清除者; 神經保護劑; Brain ischemia; Nitric oxide; Free radical scavengers; Neuroprotective agents; |
語 文 | 英文(English) |
中文摘要 | 背景:一氧化氮(NO)被報告於大腦缺血時扮演著神經保護與神經毒性的雙重角色。自由離子補捉物則在大腦缺血時據有保護大腦組織的功能。因此我們檢測一氧化氮補捉物2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO)在大鼠與小鼠永久性中大腦動脈阻塞時的神經保護作用。方法:我們使用中大腦動脈(middle cerebral artery, MCA)永久性梗塞的動物模式。在誘發中大腦動脈阻塞前一個小時,31隻Sprague-Dawley大鼠分別在腹腔內注射carboxy-PTIO (0.3, 0.6mg/kg)或生理食鹽水。另一個實驗,則使用49隻C57BL/6NCrj小鼠進行誘發中大腦動脈阻塞之後30分鐘,於腹腔注射carboxyl-PTIO (0.6, 1.2mg/kg)或生理食鹽水。於22-24小時之後,評估神經行為分數,及用2,3,5-triphenyltetrazolium (TTC)腦部染色切片定量影像分析梗塞範圍。結果:實驗結果顯示事先於大鼠發生中大腦動脈阻塞前一小時給予0.6 mg/kg carboxy-PTIO腹腔內注射,有效的降低梗塞面積的範圍(實驗組19.9±2.9%;n=10 vs.控制組29.2±2.7%;n=16),但在0.3mg/kg劑量則無差異(28.3±8.4%; n=5)。另一小鼠實驗於發生中大腦動脈阻塞後30分鐘給予0.6 mg/kg carboxy-PTIO (30.3±3.9%; n=16),亦有效降低梗塞面積的範圍(控制組:46.1±2.8%;n=18)。結論:初步的研究結論為在中大腦動脈永久性梗塞造成的局部大腦缺血,不管事先於大鼠或事後於小鼠模式給予0.6 mg/kg carboxy-PTIO皆可提供神經保護作用。 |
英文摘要 | Background: Nitric oxide (NO) has been shown to play a dual role as a neuroprotectant and a neurotoxin in cerebral ischemia. Free radical scavengers protect brain tissue from ischemic injury. Consequently, we examined the neuroprotective action of NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO), in cerebral ischemia induced by permanent middle cerebral artery occlusion (MCAO) in rats and mice. Methods: All experiments were performed in a randomized fashion. In the first series of experiments, adult Sprague-Dawley rats (n=31) subjected to permanent MCAO were treated with carboxy-PTIO (0.3, 0.6 mg/kg) or vehicle (normal saline) injected intraperitoneally (IP) 1 hr before permanent MCAO. In the second series of experiments, adult C57BL/6NCrj mice (n=49) were treated with carboxy-PTIO (0.6, 1.2 mg/kg) or vehicle saline 30 min following MCAO. Neurobehavioral scores were determined 22-24 hr following permanent MCAO and infarct volumes determined by quantitative image analysis of 2,3,5-triphenyltetrazolium (TTC)-stained brain sections. Results: Pre-treatment with carboxy-PTIO at 0.6 mg/kg IP in rats significantly attenuated infarct volume (19.9±2.9%; n=10) as compared with vehicle-treated controls (29.2±2.7%; n=16), but not at 0.3 mg/kg (28.3±8.4%; n=5). Post-MCAO treatment in mice with 0.6 mg/kg carboxy-PTIO (30.3±3.9%; n=16) significantly attenuated infarct volume as compared with vehicle-treated controls (46.1±2.8%; n=18). Conclusions: These data demonstrate that NO scavenger, carboxy-PTIO, provides significant ischemic neuroprotection when given as a pre-treatment as well as after the onset of permanent focal ischemia in two animal species. |
本系統中英文摘要資訊取自各篇刊載內容。