摘要
目的:探讨1,6-二磷酸果糖(FDP)对外伤性脑组织继发性损害的保护作用及其机制。方法:用Wistar大鼠制作脑外伤模型,于脑损伤后6小时测定血液和脑组织中丙二醛和SOD含量及血糖和C肽含量,对脑组织标本进行光镜和电镜检查。结果:FDP使脑组织和血浆中丙二醛含量下降,并能维持脑组织SOD活性。增加红细胞SOD活力,抑制血糖升高,降低血C肽水平,使神经元和胶质细胞水肿及线粒体损害减轻。结论:FDP对脑外伤后脑组织的继发性损害具有一定的保护作用,此作用与其降低脑外伤后的脂质过氧化反应、抑制血糖升高、改善线粒体对氧的利用以及稳定生物膜的作用等有关。
To discuss the protective effect of 1,6-fructose diphosphate(FDP)on secondary damage in brain injury and its mechanism. Methods:Six hours after brain injury,the contents of lipoperoxide(MDA)and superoxide dismutase(SOD)in blood and brain tissue as well as glucose and C-peptide in blood of Wistar species rates were examined. The brain tissue samples were checked under light and electric microscope. Results:FDP made the MDA contents of brain tissues and plasma and the c-peptide level in serum dropped,inhibited blood glucose elevation,kept the SOD activity of brain in a high level and increased the SOD activity of erythrocyte so as to lighten the edema of neuron and gliocyte and the damage of mitochondrion. Conclusion:FDP is of a certain protective effect on secondary damage in brain injury. This effect is related to reducing the li-poperoxidized reaction,inhibiting blood glucose elevation, improving oxygen utilization of mitochondrion and stabilizing bi-omembrane.
出处
《天津医药》
CAS
2000年第11期668-670,共3页
Tianjin Medical Journal