【摘要】目的 探讨1、6二磷酸果糖（FDP）对大鼠脑缺血/再灌注（I/R）损伤的作用及其机制。方法 雄性SD大鼠90只，随机分为三组：假手术对照组（C组）、脑缺血组（I组）、果糖组（F组），每组30只。I组和F组大鼠在凝断双侧推动脉24小时后夹闭双侧颈总动脉5分钟后重新开放，制作全脑缺血模型，C组只暴露不凝断锥动脉和不夹闭颈总动脉，F组再灌注开始时静脉注射1、6-二磷酸果糖1.5ml/kg，I组及C组分别静脉注射生理盐水1.5ml/kg。各组在再灌注后2h、6h、12h、24h、48h、72h时取标本，测定血SOD、MDA含量，并制备脑组织病理切片，采用免疫组织化学染色方法及TUNEL细胞原位凋亡检测法测定P38蛋白和Ref-1蛋白的表达和凋亡细胞数目。结果 与C组的比较，I组在再灌注后各时点SOD活性明显降低，MDA含量明显升高（P<0.05），F组变化不明显，但较I组比较均有显著差异（P<0.05）；与C组比较，I组凋亡细胞显著增多（P<0.05）；免疫组化染色显示：与C组比较，I组在再灌注后各时点P38、Ref-1表达均显著增强（P<0.05），F组较C组表达增强但较I组表达显著减弱（P<0.05）。结论 1、6-二磷酸果糖对全脑I/R损伤有保护作用，其机理可能与其参与细胞信号转导减弱P38、Ref-1蛋白表达强度有关。
【关键词】 1、6-二磷酸果糖；脑；缺血/再灌注损伤

The protective effects of FDPagainst ischemia reperfusion injury in rat brains
Xue Li, Cai ying min Xue rongliang
Anesthetic Department, the second hospital of Xi’an Jiao Tong University 710004 China
[Abstract] Objective To observe the protective effects of FDP on ischemia reperfusion in rat brains and study its mechanism. Method Healthy 90 rats were randomly divided into 3 groups: sham (group C), Is-Rs(group I), FDP(group F). 30 in one group. The rats’ two carotis were closed after two vertebralis were cut for 24h and opened for 5 minutes in group I and F, the global cerebral ischemia reperfusion model of rats were made. The rats’ vertebralis weren’t cat and carotis communis weren’t closed, FDP 1.5ml/kg was injected into veins when Is-Re began, sodium chloride 1.5ml/kg was injecteo into veins in grou免费论文网 【http://www.51lunwen.net】p I and group C. The samples were picked up at the points of 2h, 6h, 12h, 24h, 48h, 72h after reperfusion, SOD and MDA were measured with immunohistochemical methods, the expression of p38 and Ref-1 and numbers of apoptosis cells were measured with TUNEL. Result: Compared with group C, the activity of SOD at each point decreased MDA increased obviously(P<0.05) after reperfusion in guoup I. The change in group F wasn’t obviously, but Compared with group I, there was great difference (P<0.05), immunohistochemical method showed: Compared with group C, the expression of p38、Ref-1 increased after reperfusion in group I (P<0.05), the expression increased in group F compared with C, but decreased compared with group I (P<0.05), Conclusion: FDP has pretective effects on global ischemia reperfusion jnjury in rats. The mechanism of which might be its decreasing the expression of p38、Ref-1 by participating in cell signal transduction.
[Key words] FDP; brain; I/R
1、6-二磷酸果糖是细胞代谢赋活剂，可维持细胞正常极化状态，增加无氧代谢时ATP含量，通过提供离子泵能量，阻止Ca2+内流，防止活性氧族产生以及维持细胞内Ca2+和Na+正常范围。大量文献报道，其对心肌缺血有明确保护作用，但对脑缺血损伤是否有保护作用以及其作机理尚无定论。近年研究表明，MAPK信号转导通路参与脑缺血再灌注损伤，P38、Ref-1是信号转导通路中的两个蛋白，其表达的改变能间接反映脑缺血再灌注损伤的程度，故本研究拟观察1、6-二磷酸果糖对大鼠脑缺血再灌注损伤过氧化物歧化酶活性（SOD）、丙二醛（MDA）含量及凋亡细胞数目、P38蛋白、氧还因子-1（Ref-1）表达的影响，旨在探讨1、6-二磷酸果糖对脑缺血再灌注损伤的保护作用及机制。
材料与方法
90只雄性SD大鼠，由西安交通大学医学院动物中心提供，体重275~325g，随机分为3组：假手术组（C组）、缺血组（I组）、1、6-二磷酸果糖组（F组），每组30只，每组又分6个时点，每个时点随机取5只大鼠进行实验。
I组和F组大鼠凝断双侧椎动脉24h后，夹闭双侧颈总动脉5min后重新开放，用四血管法（4-VO）[1]制备全脑I/R损伤 本文来自：免费论文网 [http://www.51lunwen.net]