甲基强的松龙抑制颅脑外伤后核因子κB的表达  

Methylprednisolone inhibited the cortical NF-κB expression after human traumatic brain injury

作　　者：陈罡[1] 杭春华[1] 史继新[1] 王汉东[1] 张鑫[1] 李劲松[1] 印红霞[1] 

机构地区：[1]南京军区南京总医院神经外科,江苏南京210002

出　　处：《中华神经外科疾病研究杂志》2006年第5期399-402,共4页Chinese Journal of Neurosurgical Disease Research

摘　　要：目的探讨核因子κB(NF-κB)在人创伤性脑损伤(TBI)后挫伤皮层中的表达情况,同时观察甲基强的松龙对其表达的影响。方法挫伤区皮层的标本来自于24位TBI患者,分为两组,一组为TBI组,一组为甲基强的松龙治疗组,取样时间从伤后5h到24h。采用凝胶电泳迁移分析法(EMSA)测定NF-κB的活性,采用免疫组化技术检测NF-κBp65的表达情况。结果在人TBI后的挫伤区皮层中,NF-κB活性和表达强度明显上调,接受甲基强的松龙治疗的患者,其NF-κB活性和表达强度明显下降。结论NF-κB在人TBI后的挫伤区皮层中表达上调,提示其可能在TBI后的病理生理过程中起着重要作用,甲基强的松龙能抑制人TBI后挫伤区皮层中NF-κB的表达。Objective To analyze the expression of nuclear factor-kappa B（NF-κB） in contused human brain tissues after traumatic brain injury （TBI） and the pharmic effect of intravenous methylprednisolone on the expression of NF-κB. Methods Contused brain tissue specimens were obtained from 24 patients undergoing surgery for brain contusion 5 h to 24 h after trauma. The patients were randomly divided into the TBI group and the TBI-methylprednisolone group. The binding activity of NF-κB and the expression of NF-κB p65 were detected by electrophoretic mobility shift assay （EMSA） and immunohistochemistry methods respectively. Results The results showed an immediate and strong up-regulation of NF-κB in the area surrounding the injured brain. As compared with the TBI group, the binding activity and the expression of NF-κB were lower in the TBI- methylprednisolone group. Conclusion The results suggest that NF-κB is up-regulated obviously in the early stage after human brain contusion, NF-κB may play an important role in the pathophysiological course after TBI, and methylprednisolone can inhibit the cortical NF-κB expression after human TBI.

关 键 词：创伤性脑损伤 核因子ΚB 甲基强的松龙 

分 类 号：R651.15[医药卫生—外科学]