期刊文献+

内毒素性休克大鼠脑组织和血浆神经球蛋白水平的变化

Changes in expression of neuroglobin in brain tissues and plasma in a rat model of endotoxic shock
原文传递
导出
摘要 目的评价内毒素性休克大鼠脑组织和血浆神经球蛋白(Ngb)水平的变化。方法健康清洁级SD大鼠70只,7周龄,雌雄不拘,体重250~300g,随机分为2组:对照组(C组,n=10)和内毒素性休克组(ES组,n=60)。ES组经尾静脉注射内毒素16mg/kg制备内毒素性休克模型,C组注射等容量生理盐水。ES组于注射内毒素后3,6、12、24、48和72h(T1-6)时取颈静脉血和脑脊液(CSF)标本,随后处死大鼠,取额叶皮质和海马组织,采用ELISA法和Western blot法测定血浆、CSF、额叶皮质和海马组织Ngb的表达水平,并计算脑水含量。结果与C组比较,ES组T2-6时血浆、CSF、海马和额叶皮质Ngb水平和脑水含量升高(P〈0.01);与T2时比较,ES组T3-6时Ngb水平和脑水含量升高(P〈0.01);与T5时比较,ES组T2~4时Ngb水平和脑水含量降低(P〈0.01),T6时差异无统计学意义(P〉0.05);脑水含量与血浆、CSF、海马和额叶皮质Ngb水平呈正相关(r分别为0.631、0.719、0.707和0.706,P〈0.01)。结论大鼠内毒素性休克时机体Ngb水平上调,此变化可能是机体内源性保护机制之一。 Objective To investigate the changes in the expression of neuroglobin (Ngb) in the frontal lobe cortex, hippocampus, cerebro-spinal fluid (CSF) and plasma in a rat model of endotoxic shock. Methods Seventy SD rats of both sexes aged 7 weeks weighing 250-300 g were randomly divided into control group ( group C, n = 10) and endotoxic shock group (group ES, n = 60). LPS 16 mg/kg was injected via the vein in the tail in group ES. In group C, equal volume of normal saline was administered iv instead of LPS. Blood and CSF samples were taken and frontal lobe cortex and hippocampus were removed at 3, 6, 12, 24, 48, and 72 h after LPS administration for determination of Ngb expression by ELISA and Western blotting. Cerebral water content was measured -brain water content = (wet weight - dry weight) + wet weight× 100%. Results The brain water content was significantly increased after LPS administration and peaked at 48 h after LPS. The expression of Ngb was significantly higher in group ES than in group C and peaked at 48 h after LPS ( P 〈 0.01 ). Conclusion The up-regulation of Ngh induced by endotoxic shock is time-dependent and is one of the endogenous neuron-protective mechanisms of endotoxic shock.
出处 《中华麻醉学杂志》 CAS CSCD 北大核心 2009年第8期725-728,共4页 Chinese Journal of Anesthesiology
基金 国家自然科学基金(30270437,30771109) 教育部春晖计划(2003-26)
关键词 球蛋白类 休克 脓毒性 Globulins Shock, septic
  • 相关文献

参考文献21

二级参考文献60

共引文献49

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