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[1]梁锦屏,王琳琳,黄 菱,等.内毒素血症小鼠肺组织损伤及血清炎症因子变化的研究[J].宁夏医科大学学报,2010,(08):852-855.
 LIANG Jin-ping,WANG Lin-lin,HUANG Lin,et al.Changes of Lung Injury Indices and Serum Inflammatory Factors in Mice with Endotoxemia Induced by Lipopolysaccharide[J].Ningxia Medical University,2010,(08):852-855.
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内毒素血症小鼠肺组织损伤及血清炎症因子变化的研究(PDF)
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《宁夏医科大学学报》[ISSN:1005-8486/CN:64-1029/R]

卷:
期数:
2010年08期
页码:
852-855
栏目:
论著
出版日期:
2011-12-30

文章信息/Info

Title:
Changes of Lung Injury Indices and Serum Inflammatory Factors in Mice with Endotoxemia Induced by Lipopolysaccharide
作者:
梁锦屏1 王琳琳2 黄 菱1 郭凤英1 周 娅1
1.宁夏医科大学基础医学院病原生物学与免疫学系,银川 750004; 2. 宁夏医科大学附属医院中心实验室,银川 750004
Author(s):
LIANG Jin-ping WANG Lin-linHUANG Linet al
1.Dept. of Pathogenic Biology and Immunology, Ningxia Med. Univ., Yinchuan; 2.Dept of Med. Lab.,the Affiliated Hospital of Ningxia Med.Univ.,Yinchuan 750004
关键词:
内毒素 急性肺损伤 TNF-α NO
Keywords:
lipopolysaccharide acute lung injury tumor necrosis factor-a nitric oxide
分类号:
R373.
DOI:
-
文献标志码:
A
摘要:
目的 建立内毒素血症小鼠模型,观察模型小鼠肺损伤指标及血清炎症因子的变化,以用于抗内毒素药物研究。方法 BALB/c小鼠分为正常对照组、LPS模型组,每组再分为2、6、12 、24h四个时间点组,每组10只。LPS 7mg·kg-1尾静脉注射建立内毒素血症小鼠模型,记录一般状况、肉眼及光镜观察肺组织的病理变化; 检测肺水含量; 放免法检测血清TNF-α含量; 硝酸还原酶法检测血清NO含量。结果 内毒素肺损伤模型组小鼠在给予LPS后30min即有症状出现,至24h未见缓解; 肉眼与光镜观察肺脏病理改变,发现6h起肺脏病理改变明显可见并逐渐加重,延至24h亦未见减轻; 模型鼠肺组织W/D值显著升高; 血清TNF-α和NO值均在给予LPS后2h即显著升高,并分别在6h 和12h达到高峰,直至24h仍明显高于正常对照组(P<0.01)。结论 尾静脉注射LPS 7mg·kg-1可建立较为理想的急性肺损伤动物模型; 炎症介质的失控性表达是内毒素引起急性肺损伤的重要机制之一。
Abstract:
Objective To establish the endotoxemia model induced by lipopolysaccharide(LPS)in mice,and to observe the changes of lung injury indices and serum inflammatory factors. Methods The BALB/c mice were divided into two groups randomly, normal control group and LPS-induced model group. Each group was further divided into four subgroups by time control point. General symptoms were recorded. Histopathological changes in lung was observed and lung wet/dry weight were measured. Serum TNF-α and NO were measured by using radio immunoassay and nitrate reductase method. Results(1)Symptoms appeared at 30min after LPS injection on mice in LPS-induced model group and continued within 24h; pathological change was distinct in every time-control-point. The lung tissue pathological changes aggravated at 6h and continued within 24h. Lung wet/dry weight significantly increased in model group compared to that in controls. The levels of serum TNF-α and NO increased at 2h after LPS administration, peaked at 6h and 12h, then declined. The levels of serum TNF-α and NO sustained higher in model group than those in control group at 24h(P<0.01). Conclusion 7mg·kg-1 LPS with intravenous injection can establish an ideal animal model of acute lung injury; uncontrolled expression of inflammatory mediators is one of an important mechanism in LPS-induced acute lung injury.

参考文献/References:

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备注/Memo

备注/Memo:
收稿日期:2010-09-17 基金项目:国家自然科学基金(30660227); 教育部新世纪优秀人才支持计划(NCET-06-0916); 宁夏自然科学基金(NZ0783); 宁夏医科大学面上项目(2009年) 作者简介:梁锦屏(1977-),讲师,硕士,从事抗感染免疫研究。 通信作者:周娅(1953-),教授。E-mail:zhya29@163.com
更新日期/Last Update: 2010-08-20