摘要
目的观察弥漫性脑损伤后大鼠肠黏膜结构的动态病理变化,探讨核转录因子κB(NFκB)激活在肠黏膜屏障功能障碍中的作用。方法采用Marmarou模型致大鼠重型弥漫性脑损伤。150只雄性Wistar大鼠随机分成对照组和伤后1、2、4、8、12、24、48、72、168h9个时间点组。在光镜下检测对照组及伤后不同时间点大鼠小肠黏膜厚度及绒毛高度和宽度的变化,利用免疫组化技术检测NFκB在伤后不同时间点组中的表达。结果各致伤组小肠黏膜厚度及绒毛高度和宽度均明显低于对照组(P<0.05或P<0.01)。免疫组化显示:各致伤组NFκB表达的积分吸光度值均显著大于对照组(P均<0.01)。结论弥漫性脑损伤后,早期光镜下即有肠黏膜组织结构的受损表现,损伤诱导细胞应激激活NFκB,这一作用可能参与肠道继发性损害的发生。
Objective To investigate the dynamic pathological changes in the intestinal mucosa of rats and the role of activation of nuclear factor -κB (NF-κB) in the alteration in intestinal mucosal barrier dysfunction after diffuse brain injury. Methods The animal model established by Marmarou was used to produce diffuse brain injury. One hundred and fifty male Wistar rats were randomly divided into nine groups in terms of postinjury time : 1, 2, 4, 8, 12, 24, 48, 72, 168 hours after injury, and control group. Mucosal thickness, villous height and width were estimated under light microscope, and expression of NF-κB was assessed with immunohistochemical staining in control group to compare with those in injury groups. Results Mucosal thickness, villous height and width were diminished and the optical density of expression of NF-κB was much higher in the injury groups than those of control group. Conclusion The structure of intestinal mucosa is damaged in the earlier stages after diffuse brain injury. NF-κB is activated by cellular stress, which may be involved in the pathogenesis of secondary intestinal lesion.
出处
《中国危重病急救医学》
CAS
CSCD
北大核心
2005年第9期555-557,F0006,共4页
Chinese Critical Care Medicine
基金
河北省科研计划项目(032761133)