Zhou Jian-ping, Wang Fan, Li Rui-lin, Yuan Bao-li, Li Jing, Xu Er-di
Department of Pediatrics, the Second Hospital of Xi'an Jiaotong University, Xi'an 710004, China.
Zhonghua Er Ke Za Zhi. 2004 Feb;42(2):129-33.
Febrile seizure (FS) is a pediatric emergency. The reiterative attacks of FS may result in brain damage to various extents. Fructose-1,6-diphosphate, serving as a cellular energy substance, has been applied to clinical practice for many years and has shown its importance in adjuvant treatment of diseases with myocardial damage. This study aimed to explore the potentiality of protecting rats' brain damage caused by febrile seizure with fructose-1,6-diphosphate (FDP).
Thirty 21-day-old male Sprague-Dawley (SD) rats were randomly divided into febrile seizure group (FS), sodium chloride solution (NS) control group and FDP intervention group (FD). Febrile seizure was induced by hyperthermal bath at 45 degrees C in the present study. No intervention treatment was given to rats in FS group before febrile seizure. Thirty minutes before febrile seizures, rats in FD group were given peritoneal injection of FDP at a dose of 25 mg per 100 g of body weight, whereas the same volume of 0.9% sodium chloride solution was injected into peritoneum of rats in NS group. Manifestations of seizure and differences in seizure latency, duration of seizure and seizure severity were observed in all the 3 groups. Samples of rat brain were prepared for electron microscopy in order to understand the characteristics of the ultrastructural changes in mitochondria, interspace of neuronal synapses and neurons of hippocampal region CA(1).
Data collected from this study indicated that peritoneal injection of FDP at 25 mg per 100 grams of body weight 30 minutes before febrile seizures could result in improvement of the clinical manifestation of the rats caused by febrile seizures. Specifically speaking, the seizure latency was prolonged, the duration of seizures was shortened and severity of seizure was reduced. Analysis of variance and q-test on the data collected from the 3 groups revealed that there were significant differences between FD group and the other two groups (P < 0.05), yet no significant difference was found between FS group and NS group (P > 0.05). Electron microscopic observations on brain specimens revealed that FDP could relieve mitochondrial degeneration and edema. FDP could also reduce neuronal degeneration and necrosis in hippocampal region CA(1) (the percentages of neuronal degeneration and necrosis in the 3 groups were respectively 13% for FD group, 28% for FS group and 30% for NS group). There was a significant difference between FD group and the other two groups (P < 0.05), FDP treatment could prevent interspace of neuronal synapses from enlarging (the mean interspace was 6.47 +/- 0.37 micro m for FD group, 7.60 +/- 0.36 micro m for FS group and 7.53 +/- 0.40 micro m for NS group. The difference between FD group and the other two groups was significant (P < 0.01).
FDP could lead to prolonged seizure latency, shorter duration of seizures and mitigation of seizures severity. FDP could also reduce neuronal degeneration and necrosis and prevent the interspace of neuronal synapses from enlarging in hippocampal region CA(1). The present study suggests that FDP can protect brain of rat from damages caused by febrile seizures.
热性惊厥（FS）是一种儿科急症。FS的反复发 作可能会在不同程度上导致脑损伤。1,6-二磷酸果糖作为一种细胞能量物质，已应用于临床实践多年，并在心肌损伤疾病的辅助治疗中显示出其重要性。本研究旨在探讨1,6-二磷酸果糖（FDP）对热性惊厥所致大鼠脑损伤的保护潜力。
将30只21日龄雄性Sprague-Dawley（SD）大鼠随机分为热性惊厥组（FS）、氯化钠溶液（NS）对照组和FDP干预组（FD）。本研究通过45℃热浴诱导热性惊厥。FS组大鼠在热性惊厥前未给予干预治疗。在热性惊厥前30分钟，FD组大鼠腹腔注射剂量为每100g体重25mg的FDP，而NS组大鼠腹腔注射相同体积的0.9%氯化钠溶液。观察3组大鼠的惊厥表现以及惊厥潜伏期、惊厥持续时间和惊厥严重程度的差异。制备大鼠脑样本用于电子显微镜检查，以了解海马区CA(1)线粒体、神经元突触间隙和神经元超微结构变化的特征。
本研究收集的数据表明，在热性惊厥前30分钟腹腔注射每100克体重25mg的FDP可改善大鼠热性惊厥所致的临床表现。具体而言，惊厥潜伏期延长，惊厥持续时间缩短，惊厥严重程度降低。对3组收集的数据进行方差分析和q检验显示，FD组与其他两组之间存在显著差异（P<0.05），而FS组与NS组之间未发现显著差异（P>0.05）。脑标本的电子显微镜观察显示，FDP可减轻线粒体变性和水肿。FDP还可减少海马区CA(1)神经元的变性和坏死（3组神经元变性和坏死的百分比分别为FD组13%、FS组28%、NS组30%）。FD组与其他两组之间存在显著差异（P<0.05），FDP治疗可防止神经元突触间隙扩大（FD组平均间隙为6.47±0.37μm，FS组为7.60±0.36μm，NS组为7.53±0.40μm。FD组与其他两组之间的差异显著（P<0.01）。
FDP可导致惊厥潜伏期延长、惊厥持续时间缩短和惊厥严重程度减轻。FDP还可减少神经元变性和坏死，并防止海马区CA(1)神经元突触间隙扩大。本研究表明，FDP可保护大鼠脑免受热性惊厥所致的损伤。
