摘要
目的探讨锌原卟啉(ZnPP)对高热惊厥(FC)发育期大鼠血红素氧合酶(HO)-1mRNA表达的影响及作用机制。方法65只21日龄Wistar大鼠,随机分为对照组、高热未惊厥组、FC组及ZnPP治疗组。采用热水浴(每次5min,隔日1次,共10次)诱导FC大鼠动物模型;ZnPP治疗组于制备FC模型前腹腔注射ZnPP45μmol/kg。取大鼠脑组织制作冷冻切片,用组织原位杂交技术观察大鼠海马CA1、CA3区和齿状回DG区HO-1mRNA表达。结果FC组大鼠海马CA1、CA3区及齿状回HO-1mRNA表达显著增强,与ZnPP治疗组、高热未惊厥组及对照组比较均有显著性差异(Pa<0.01)。ZnPP治疗组HO-1mRNA表达显著高于高热未惊厥组及对照组(Pa<0.01)。结论FC能引起HO-1mRNA过度表达;ZnPP能通过下调HO-1mRNA表达对FC脑损伤起保护作用。
Objective To explore the effect of Znic Protoporphyrin （ZnPP） and its mechanism on the hemeoxygenase - 1 （ HO - 1 ） mRNA expression in brain tissue of developing rat with febrile convulsion （FC）. Methods Sixty - five 21 - day Wistar rats were randomly divided into 4 groups： control group（ n = 14）, none - FC group （ n = 16） , FC group（ n = 20） and ZnPP treated groups（ n = 15 ）. FC in rats was induced 10 times ,once every 2 days in a bath of warm water. ZnPP treated group were received ZnPP 45 μmoL/kg before FC models. The expressions of HO - 1 mRNA were detected in hippocampal CA1, CA3 and dentate gyms with the technique of hybridization in situ. Results The expressions of HO - 1 mRNA significantly increased in hippocampal CA1, CA3 region and dentate gyms in FC group compared with those in control group, none FC group and ZnPP treated group （Pa 〈 0.01 ）. And the HO - 1 expression in ZnPP -treated group was significantly higher than that of none FC group and control group （ Pa 〈 0.01 ）. Conclusions Recurrent FC in rats can cause the increase of HO - 1 mRNA expression ; ZnPP probably plays a role in protecting the brain from FC damage by down - regulating the HO - 1 mRNA expression.
出处
《实用儿科临床杂志》
CAS
CSCD
北大核心
2007年第16期1261-1262,1266,共3页
Journal of Applied Clinical Pediatrics
基金
黑龙江省教育厅科学技术研究重点项目资助(11511400)
