摘要
目的:研究创伤性脑损伤(TB I)后肠组织核因子-κB(NF-κB)和基质金属蛋白酶-9(MMP-9)的表达,探讨其在肠黏膜屏障损害中的作用机制。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成年大鼠36只,随机分为对照组、TB I后3、12、24、72 h和7 d组,每组各6只。采用凝胶电泳迁移(EMSA)法测定NF-κB的活性,免疫组化测定MMP-9的表达。结果:TB I后肠组织NF-κB的活性和MMP-9的表达逐渐增强,TB I后72 h达高峰,至伤后7 d仍保持较高水平。NF-κB和MMP-9在表达时相和强度上基本一致。MMP-9的表达主要位于绒毛固有膜、隐窝和黏膜下层,阳性细胞包括血管内皮细胞、淋巴细胞和中性粒细胞。结论:TB I可引起肠组织NF-κB活性和MMP-9的表达明显增强,可能在肠黏膜屏障损害中起重要作用。
Objective：The aim of the current study was to investigate the expression of nuclear factor-κB （NF-κB） and metalloproteinase-9 （MMP-9） in the small intestine and to explore the potential role of NF-κB and MMP-9 in the damage of gut mucosal barrier after traumatic brain injury. Methods：The trauma was produced by a free-falling weight on the exposed dura of right parietal lobe. The rats were randomly divided into control group and traumatic brain injury groups at hours 3, 12, 24 and 72, and on day 7. NF-κB binding activity in the small intestine was studied by electrophoretic mobility shift assay （EMSA）, and the expression of MMP-9 was studied by immunohistochemistry. Results：The results showed that NF-κB binding activity and MMP-9 expression in the small intestine was progressively increased, reached the maximum at 72 h and kept at high level up to 7 d after TBI. Concomitant upregula- tion of NF-κBand MMP-9 was observed. MMP-9 positively immunostained cells were mainly located at villous interstitium, lamina propria, crypt and submucosal layer, including endothelial cells, lymphocytes and neutrophils. 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 small intestine which might play a central role in the damage of gut mucosal barrier.
出处
《医学研究生学报》
CAS
2006年第12期1073-1076,I0018,共5页
Journal of Medical Postgraduates
基金
全军医学科学技术研究"十五"攻关课题基金资助(批准号:06G041)
