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作 者:杭春华[1] 史继新[1] 吴伟[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:《创伤外科杂志》2006年第5期398-401,共4页Journal of Traumatic Surgery
摘 要:目的研究创伤性脑损伤(TB I)后损伤区脑组织核因子κB(NF-κB)和基质金属蛋白酶-9(MMP-9)的表达,探讨其在继发性脑损害中的作用机制。方法采用自由落体撞击法造成大鼠右侧顶叶脑挫裂伤,W istar大鼠随机分为对照组、伤后3、12、24、72小时和7天组。采用EMSA测定NF-κB的活性,免疫组化测定MMP-9的表达。结果TB I后NF-κB的活性和MMP-9的表达逐渐增强,至伤后72小时达高峰,伤后7天仍保持在较高水平。NF-κB和MMP-9在表达时相和强度上呈正相关关系。MMP-9表达阳性细胞包括血管内皮细胞、神经胶质细胞和少数神经元细胞及侵入的中性粒细胞。结论TB I可引起损伤区脑组织NF-κB活性和MMP-9的表达明显增强,可能在脑组织的继发性损害中起重要作用。Objectives The aim of the current study was to investigate the nuclear factor-κB (NF-κB) binding activity and expression of metalloproteinase-9 (MMP-9 ) in the injured brain and to explore the potential role of NF-κB and MMP-9 in the secondary brain injury after traumatic brain injury(TBI). Methods The trauma was produced by a free-falling weight on the exposed dura of right parietal lobe. The rats were randomly divided into contrnl group and traumatic brain injury groups at hours 3,2, 24 and 72,and on day 7. Intraeerebral NF-κB binding activity in the injured brain was studied by electrophoretic mobility shift assay( EMSA) ,and the expression of MMP- 9 studied by immunohistochemistry. Results The results showed that NF-κB binding activity and MMP-9 expression in the injured site progressively increased,reached the maximum at 72h and kept at high level up to 7 d after TBI. Concomitant upregulation of NF-κB and MMP-9 was observed in the injured brain and there was a high positive relation between two variables. MMP-9 positively immunostained cells included endothelial cells, neuroglial cells,few neurons and migrated leukocytes. Conclusion It was concluded that cortical contusion trauma could induce a concomitant and persistent upregulation of NF-κB binding activity and MMP-9 expression in the injured brain which might play a central role in the secondary injury after TBI.
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