1，6-二磷酸果糖对新生鼠缺氧缺血性脑损伤的保护机制研究

The protective mechanism of fructose-1,6-disphophate on the hypoxic-ischemic brain damage of neonatal rats

目的探讨1，6-二磷酸果糖（FDP）对新生大鼠缺氧缺血性脑损伤（mBD）的保护机制。方法建立新生大鼠HIBD模型，随机分为HIBD对照组、盐水处理组、FDP不同剂量治疗组，于缺氧缺血后24h利用RT-PCR方法观察脑组织caspase-3mRNA的表达变化。结果盐水处理组、H]BD对照组和FDP小剂量组easpase-3mRNA表达差异无统计学意义（P〉0．05），FDP大、中剂量组其表达均有不同程度的下凋，同以上三组比较差异有统计学意义（P〈0．05），FDP大、中剂量组相比差异无统计学意义（P〉0．05）。结论FDP对HIBD的神经保护机制可能与下调caspase-3mRNA表达有关，进而抑制神经细胞凋亡。

Objective To explore the protective mechanism of fructose-1, 6-disphophate on the hypoxie- ischemie brain damage of neonatal mrs. Methods Seven-day-old Wistar mrs were randomly divided into HIBD control group,sallne-treated group, FDP-treated group. FDP-treated group was redivided into groups of high, middle and low dese.The expression of caspase-3mRNA was detected at 24h after HIBD with RT-PCR. Results There were no sifnificant differences of the caspase-3 mRNA expression among tile saline-treated group, HIBD group and low dose FDP-treated group（ P 〉 0.05）. The expressions of easpase-3 mRNA in the middle and high dose FDP-treated groups decreased significantly as campared to the above three groups （ P 〈 0.05 ）, but there was no significant difference between the two groups（ P 〉 0.05 ）. Conclusion The neuronal protective mechanism of FDP might be related to downregulate the gene expression of caspase-3 in brain tissue,and decrease the apoptosis of neuron after HIBD.