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目的探讨内源性血红素氧合酶(HO)一氧化碳(CO)系统对反复热性惊厥(febrile seizures,FS)脑损伤的影响。方法21日龄SD大鼠24只,随机分为3组:对照组、FS组和FS+锌原卟啉Ⅸ(ZnPPⅨ)组。采用热水浴诱导大鼠FS,隔日诱导1次,共诱导10次。用双波长分光光度计间接测定大鼠血浆中CO含量;记录大鼠惊厥强度、潜伏期、持续时间及惊厥时的肛温;HE染色观察海马神经元形态学改变;电镜观察海马神经元超微结构的改变;尼氏染色对海马神经元进行半定量计数分析。结果反复FS后,血浆CO含量明显高于对照组,FS+ZnPPⅨ组血浆CO含量较FS组低,与对照组比较无统计学意义;随着惊厥次数的增加,FS组大鼠惊厥持续时间呈延长趋势,FS+ZnPPⅨ组大鼠惊厥潜伏期呈缩短趋势,惊厥持续时间较FS组长,惊厥强度和惊厥时的肛温两组差异无统计学意义;反复FS后,光镜和电镜下均发现海马神经元出现损伤改变,ZnPPⅨ的干预加重了神经元的损伤;反复FS后未见海马神经元的丢失,ZnPPⅨ的干预导致了神经元的显著丢失。结论内源性HO CO系统对反复FS脑损伤发挥着重要的保护作用。
Objective To investigate the effect of endogenous heme oxygenase (CO) system on brain injury induced by febrile seizures (FS) in rats. Methods Twenty-four SD rats aged 21 days were randomly divided into three groups: control group, FS group and FS + ZnPPⅨ group. The rat was induced by hot water bath, induced once a day for a total of 10 times. The contents of CO in plasma of rats were measured indirectly by dual-wavelength spectrophotometer. The convulsive intensity, latency, duration and anal rectal temperature were recorded. The morphological changes of hippocampal neurons were observed by HE staining. The ultrastructure of hippocampal neurons was observed by electron microscopy The changes of hippocampal neurons were analyzed by Nissl staining. Results After repeated FS, plasma CO levels were significantly higher than the control group, FS + ZnPPⅨ plasma CO levels lower than the FS group, compared with the control group was not statistically significant; with the increase in the number of seizures, FS group convulsions duration was The lengthening tendency showed that the latent period of convulsion in FS + ZnPPⅨ group was shortened, and the duration of convulsion was no significant difference compared with those in FS group, seizure intensity and rectal temperature. After repeated FS, the convulsions were found under light and electron microscope Changes of hippocampal neurons damage, ZnPPⅨ intervention increased neuronal damage; repeated FS no hippocampal neuronal loss, ZnPPIX intervention resulted in a significant loss of neurons. Conclusion The endogenous HO CO system plays an important role in the protection of recurrent FS brain injury.