CAJ | 학술논문

目的：研究高迁移率族蛋白-1（HMGB-1）在戊四氮（PTZ）致幼鼠癫痫（EP）后在不同脑区的变化，探讨EP发作后脑组织的损伤情况。方法40只21日龄幼年雄性SD大鼠，随机分对照组（A组，8只）及实验组（32只）。实验组按体质量40 mg/kg腹腔注射PTZ ，对照组腹腔注射与致痫剂同等容量的生理盐水。根据EP发作后的时间，随机于其发作后1 h（B组）、6 h（C组）、24 h（D组）、72 h（E组）取脑，采用免疫组织化学方法，观察各组大鼠海马组织中 HMGB-1的改变；RT-PCR方法观察各组大鼠额叶、海马、中脑中 HMGB-1的变化。结果EP发作后，幼鼠额叶、海马、中脑HMGB-1的表达随着时间的推移呈动态升高，其中额叶、海马HMGB-1蛋白于发作6 h后开始升高，24 h达高峰，72 h逐渐下降，其中额叶、海马在发作后6、24、72 h高于对照组，中脑升高值仅于72 h高于对照组。结论 EP发作可造成大脑损伤。
목적：연구고천이솔족단백-1（HMGB-1）재무사담（PTZ）치유서전간（EP）후재불동뇌구적변화，탐토EP발작후뇌조직적손상정황。방법40지21일령유년웅성SD대서，수궤분대조조（A조，8지）급실험조（32지）。실험조안체질량40 mg/kg복강주사PTZ ，대조조복강주사여치간제동등용량적생리염수。근거EP발작후적시간，수궤우기발작후1 h（B조）、6 h（C조）、24 h（D조）、72 h（E조）취뇌，채용면역조직화학방법，관찰각조대서해마조직중 HMGB-1적개변；RT-PCR방법관찰각조대서액협、해마、중뇌중 HMGB-1적변화。결과EP발작후，유서액협、해마、중뇌HMGB-1적표체수착시간적추이정동태승고，기중액협、해마HMGB-1단백우발작6 h후개시승고，24 h체고봉，72 h축점하강，기중액협、해마재발작후6、24、72 h고우대조조，중뇌승고치부우72 h고우대조조。결론 EP발작가조성대뇌손상。
Objective The aims of this study were to investigate the changes of HMGB1 in serum and different parts of brain of young rats with epilepsy (EP)induced by pentylenetetrazol (PTZ) ,and to evaluate the effect of epileptogenesis upon brain damage . Methods Forty healthy male SD rats around 21 days of age were randomly divided into experimental (n=32) and control (group A ,n=8) groups and they were injected intra-peritoneally with PTZ (40 mg/kg) and normal saline respectively . According to the time after seizures ,the rats were decapitated at 1 h(group B) ,6 h(group C) ,24 h(group D)and 72 h (group E) . The frontal cortex ,hippocampus and mesencephalon were collected ,and the expression lev-els of HMGB-1 and HMGB-1 mRNA in different parts of brain were detected by immunohistochemistry and real-time PCR . Results The levels of HMGB-1 gradually increased over time dynamically in frontal lobe ,midbrain and hippocampus ,of which the HMGB-1 increased at 6 h in frontal lobe and hippocampus and that showed a highest level at 24 h ,but decreased at 72 h . It was still higher than that of the control group yet . There were significant statistical differences . Meanwhile ,the level of HMGB-1 is higher than that of control group at 72 h in midbrain ,it showed significant differences . Conclusion The in-creased level of HMGB-1 may play an important role in cerebral injury induced by EP .