期刊文献+

弥漫性脑损伤后大鼠肠黏膜病理变化的动态观察及核转录因子-κB的表达 被引量:5

Dynamic observation of pathological changes and expression of nuclear factorκB in the intestinal mucosa of rats after diffuse brain injury
下载PDF
导出
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)
关键词 脑损伤 弥漫性 组织形态学 核转录因子-ΚB 肠黏膜 Wistar大鼠 弥漫性脑损伤 肠黏膜屏障 脑损伤后 病理变化 动态观察 diffuse brain injury histomorphology nuclear factor-κB intestinal mucosa
  • 相关文献

参考文献12

  • 1Kombean J L,Takala J.Summary of round table conference:gut dysfunction in critical illness[J].Intensive Care Med,1997,23:475-480.
  • 2Marmarou A,Foda M A,Brink W D,et al.A new model of diffuse brain injury in rat[J].J Neurosurg,1994,80:291-313.
  • 3王佩燕.肠——多器官功能障碍综合征防治的靶器官?[J].中国危重病急救医学,2001,13(11):647-648. 被引量:30
  • 4Abraham E.NF-κB Nuclear activation[J].Crit Care Med,2000,28:N100-N104.
  • 5Christman J W,Lancaster L H,Blackwell T S.Nuclear factor kappa-B:a pivotal role in the systemic inflammatory response syndrome and new target for therapy[J].Intentsive Care Med,1998,24:1131-1138.
  • 6顾大勇,曾祥元,陈莉,杨季云,马布仁,王天然,唐旭东,石力.LPS诱导肺微血管内皮细胞ICAM-1的表达及NF-κB作用的实验研究[J].中国微循环,2002,6(1):25-28. 被引量:19
  • 7Satoh A,Shimosegawa T,Fujita M,et al.Inhibition of nuclear factor-kappa-B activation improves the survival of rats with taurocholate pancreatitis[J].Gut,1999,44:253-258.
  • 8Hassoun H T,Kozar R A,Kone B C,et al.Intraischemic hypothermia differentially modulates oxidative stress proteins during mesenteric ischemia/reperfusion[J].Surgery,2002,132:369-376.
  • 9Russell J,Epstein C J,Grisham M B,et al.Regulation of E-selectin expression in postischemic intestinal microvasculature[J].Am J Physiol,2000,278:G878-885.
  • 10Jobin C,Sartor R B.The I-kappa-B/NFkappa-B system:a key determinant of mucosal inflammation and protection[J].Am J Physiol Cell Physiol,2000,278:C451-C462.

二级参考文献3

  • 1Hiroshi Ikeda,Chao-Long Yang,Jie Tong,Haruaki Nishimaki,Kenji Masuda,Tomohiro Takeo,Kenji Kasai,Gen Itoh. Rat Small Intestinal Goblet Cell Kinetics in the Process of Restitution of Surface Epithelium Subjected to Ischemia–Reperfusion Injury[J] 2002,Digestive Diseases and Sciences(3):590~600
  • 2顾大勇,曾祥元,马佈仁.NF-κB与微循环障碍[J].中国微循环,2001,5(1):77-79. 被引量:10
  • 3梁存河,蒋朱明.胃肠屏障研究的几个热点问题[J].中国危重病急救医学,2001,13(4):202-204. 被引量:19

共引文献61

同被引文献71

引证文献5

二级引证文献8

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部