目的　探讨 1,6 二磷酸果糖 (FDP)对缺血性脑组织损伤的保护机制。方法　利用大鼠局灶性脑缺血模型 ,采用TTC染色、免疫组织化学染色、Western印迹法和TUNEL染色技术 ,观察FDP对脑梗死面积、缺血区脱嘌呤 /脱嘧啶核酸内切酶 (APE/Ref 1)表达水平以及缺血区细胞凋亡程度的影响。结果　 1,6 二磷酸果糖可显著性减少脑梗死面积 (31 0mm2 ± 2 9mm2 与 4 7 3mm2 ± 6 0mm2 )。可减少缺血半暗带TUNEL阳性细胞数量 ,缺血 2 4h组与FDP干预组分别为 6 9 3± 2 4个 /mm2 与4 2 8± 1 7个 /mm2 。上调缺血半暗带APE/Ref 1蛋白的表达 :缺血 2 4h组与FDP干预组比较APE/Ref 1免疫阳性细胞数分别为 2 6 3± 2 9个 /mm2 与 4 7 0± 3 4个 /mm2 ;Western印迹法光密度扫描值分别为 5 3± 3 2与 13 8± 5 4。结论　FDP可通过上调脱嘌呤 /脱嘧啶核酸内切酶表达水平 ,增强脑组织对缺血损伤的修复能力 ,减少缺血半暗带细胞凋亡发生 ,阻止脑梗死范围进一步扩大 ,因而对缺血性脑损伤具有保护作用 Objective To investigate the protective mechanism of fructose 1,6 diphosphate (FDP) on ischemic brain injury. Methods Focal cerebral ischemia model was used in rats. TTC staining, immunohistochemical staining, Western blotting and TUNEL staining were used to observe the effects of FDP on cerebral infarct area, apurinic / apyrimidinic endonuclease (APE / Ref 1) expression and the extent of apoptosis in ischemic area. Results Fructose 1, 6 diphosphate could significantly reduce the infarct size (31 0mm2 ± 29mm2 and 473mm2 ± 60mm2). The number of TUNEL positive cells in ischemic penumbra could be decreased. The number of TUNEL positive cells in ischemic penumbra was 693 ± 2 4 / mm2 and 428 ± 1 7 / mm2 respectively. Upregulated the expression of APE / Ref 1 protein in ischemic penumbra: Compared with FDP intervention group, the number of APE / Ref 1 immunoreactive cells in 24 h ischemia group was 263 ± 29 / mm2 and 4700 ± 34, respectively / Mm2; Western blot optical density scans were 53 ± 32 and 13 8 ± 54, respectively. Conclusion FDP can up-regulate the expression of apurinic / apyrimidinic endonucleases, enhance the ability of brain tissue to repair ischemic injury, reduce the apoptosis of ischemic penumbra cells and prevent the further expansion of cerebral infarction. Sexual brain injury has a protective effect