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机构地区:[1]成都市第三人民医院神经外科,四川成都610031
出 处:《四川医学》2013年第2期167-169,共3页Sichuan Medical Journal
摘 要:目的探讨急性创伤性脑损伤后核转录因子-kB(NF-kB)表达变化规律,以及NF-kB特异性抑制剂PDTC能否减轻继发性脑损伤,以期为治疗颅脑损伤提供新策略。方法将Wistar大鼠随机分为3组:假手术对照组、脑损伤组及脑损伤治疗组。以免疫组织化学法观察创伤性脑损伤后NF-kB表达的变化规律及NF-kB抑制剂PDTC对脑损伤后NF-kB表达的影响。结果在脑损伤组动物的脑组织内,围绕损伤灶神经变性区,从伤后6h到120h,NF-kB表达较假手术对照组明显增高。而PDTC脑损伤治疗组,NF-kB表达较损伤组明显下降(P<0.05)。结论创伤后NF-kB表达显著增高,NF-kB激活可能是继发性脑损害的重要分子机制。PDTC可能通过抑制NF-kB表达,从而对创伤性脑损伤后继发性脑损害具有保护作用。Objective To investigate the expression of NF-kB after traumatic brain injury,and if the secondary brain injury would decrease when the expression of NF-kB was inhibited by PDTC,in order to provide the theoretical basis directly for a new approach to the clinical management of traumatic brain injury.Methods The free-falling-body impact device was used to cause the models of local moderate contusion and laceration in the rats.Sixty Wistar rats were randomly divided into three groups: control group,injury group and treatment group.Pyrro-lidinedithiocarbamate(PDTC) was given to the treatment group.Immunohistochemistry in situ detection was used to assry the expression of NF-kB after traumatic brain injury and the effect of PDTC on secondary brain injury.Results In the neurodegenerative area surrounding the lesion of injury group,a significative increasing of NF-kB was observed from 6h to 120h.In contrast,the expression of NF-kB was significantly downregulated by PDTC.Conclusion The study shows the activation of NF-kB may be the important mechanism of acute traumatic brain injury.And the NF-kB inhibitor may be a potential therapeutic method for the treatment of after traumatic brain injury.
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