摘要
目的探讨甘草甜素（GL）预处理对幼鼠癫痫模型急性期海马组织、血清中高迁移率族蛋白1（HMGB1）表达水平及慢性期海马CA1区、CA3区神经元核特异蛋白（Neu-N）表达的影响。方法52只21日龄SD大鼠按随机数字表法分为对照组（12只）、模型Ⅰ组（16只）、模型Ⅱ组（24只）。模型Ⅰ组用海人酸（KA）诱导癫痫发作，模型Ⅱ组在用KA前30min腹腔注射GL，模型Ⅰ组根据观察时间点不同分为3h、12h、24h、7d4个亚组，模型Ⅱ组根据GL不同剂量分为10mg／kg、50ms／kg、100ms／kg3个亚组，每个亚组3只。行为学表现按照Racine评分量表进行评分，实时荧光定量PCR及Westernblot检测急性海马区HMGB1 mRNA及蛋白的表达，ELISA检测血清中HMGB1蛋白的表达，免疫组织化学检测慢性期（7d）海马Neu-N的表达。结果模型Ⅱ组与模型Ⅰ组比较，癫痫发作时间明显延长[（24．08±1．98）min比（33．39±2．66）min]，差异有统计学意义（t=9．231，P〈0．05）；模型Ⅰ组与对照组比较，随着观察时间（3h、12h、24h）的延长，HMGB1的基因表达升高，在12h时达到峰值，差异有统计学意义（H=10．532，P〈0．05），HMGB1的蛋白表达改变不明显，差异无统计学意义（H=5．227，P〉0．05），血清中HMGB1水平升高，其中在12h时升高最明显，差异有统计学意义（H=6．897，P〈0．05）；在12h时间点，模型Ⅱ组与模型Ⅰ组比较，HMGB1的基因表达降低（H=10．721，P〈0．05）（100mg／kg组明显），血清中HMGB1的水平降低（H=6．967，P〈0．05）（100ms／kg组明显）；在7d时间点，模型Ⅰ组与对照组比较，海马区神经元丢失减少（P〈0．05），模型Ⅱ组与模型Ⅰ组比较，海马区神经元的丢失减少（P〈0．05）（CA1区100ms／kg组明显，CA3区50mg／kg明显）。结论在幼鼠的颞叶癫痫模型中，GL可能通过抑制HMGB1基因的合成及释放，降低胞外HMGB1水平
Objective To study the effect of glycyrrhizin（GL） on the gene expression of high mobility group protein 1 （ HMGB1 ） in hippocampus and serum. To evaluate the effect on the expression of neuron - specific nuclear - binding protein（ Neu- N） in the hippocampus CA1, CA3 regions in the chronic stage of an immature rat epilepsy model. Methods Fifty - two 21 day - old SD rats were randomly divided into control group, model group I and model group Ⅱ according to the random table method. Model group Ⅰ was induced epilepsy by kainie acid （ KA）, and the model group Ⅱ was pretreated with GL by intraperitoneal injection at 30 min before KA injection. According to the different observation time points, each group was divided into 4 subgroups ：3 h, 12 h,24 h and 7 d. Model group Ⅱ was divided into 3 subgroups ： 10 mg/kg,50 mg/kg, 100 mg/kg, according to the different doses of GL. There were 3 animals in each subgroup. Score was performed according to the Racine score, and quantitative real -time polymerase chain reac- tion and Western blot were applied to detect the mRNA and protein expression of HMGB1 in the acute phase. Enzyme - linked immunosorbent assay（ELISA） was applied to measure the expression of HMGB1 in blood;immunohistochemical was applied to measure the expression of Neu - N in hippocampus in the chronic phase（7 d）. Results Compared with model group Ⅰ , seizure onset time was obviously prolonged in model group Ⅱ [ （ 24.08 ± 1.98 ） min vs. （ 33.39 ± 2. 66） mini ,and the difference was statistically significant （t =9.231 ,P 〈0.05） ;Comparing KA model group Ⅰ with control group,the gene expression of HMGB1 significantly increased, and reached a peak at the time of 12 h （H = 10. 532, P 〈 0.05 ）, but the protein expression of HMGB1 was changed obviously and there was no significant difference （H = 5. 227 ,P 〉 0.05）. The expression of HMGB1 in the serum also significantly increased, especially at 12 h （H = 6. 897 ,P 〈0.05）. At the time of 12 h aft
出处
《中华实用儿科临床杂志》
CSCD
北大核心
2017年第14期1111-1115,共5页
Chinese Journal of Applied Clinical Pediatrics
基金
河南省高等学校重点科研项目（17A310037）
关键词
甘草甜素
海人酸
癫痫
幼鼠
高迁移率族蛋白1
神经元损伤
Glyeyrrhizin
Kainic acid
Epilepsy
Immature rat
High mobility group protein 1
Neuronal injury
