摘要
目的 探讨脂多糖(LPS)致伤大鼠后肺组织激活蛋白-1(AP-1)活性与肺组织损害及功能障碍程度的关系。方法 经Wistar大鼠尾静脉注射不同剂量(2、4、6及8mg/kg)LPS复制急性肺损伤(ALI)模型,以注射生理盐水为对照,观察致伤后不同时相点(1、2、4及6h)大鼠的呼吸频率及死亡情况;检测动脉血氧分压(PaO_2)和肺湿重/干重(W/D)值,并行组织学检查;采用凝胶迁移率分析法(EMSA)检测肺组织AP-1活性。结果 LPS 2mg/kg即可致大鼠呼吸频率增快,LPS≥6mg/kg时出现呼吸困难或呼吸窘迫,死亡率为60％(36/60);各剂量组PaO_2均较对照组低,以LPS≤6mg/kg降低显著(P<0.01);肺组织W/D用值从LPS 2mg/kg、2h时显著升高,LPS≥4mg/kg各时相均显著升高(P<0.05);肺大体观察LPS剂量越大,肺水肿及炎症反应越严重;LPS致伤后肺组织AP-1活性均升高,剂量越大,AP-1活性越高,不同剂量组均在2h点达到高峰,且以LPS≥6mg/kg组升高显著(P<0.01)。结论 ①LPS≥6mg/kg是介导大鼠发生ALI和ARDS的临界剂量;②肺组织AP-1活性升高水平与肺组织损伤和功能障碍程度密切相关。
Objective To establish the model of rat acute lung injury (ALI) induced by lipopolysaccharides(LPS) and to measure the activator protein-1 (AP-1) binding activity in lung tissue. Methods Wistar rats were injured with escalating doses of LPS to establish ALI model. Elec-trophoretic mobility shift assays(EMSAs) was employed to measure AP-1 binding activity in rat lung tissues. Results 1. The ALI could be imitated in rats with LPS. 2. Acute respiratory distress syndrome (ARDS) was induced under condition of LPSf^6 mg/kg. 3. LPS may cause increased AP-1 activity in lungs in rats and AP-1 activity increased significantly on dose of LPS≥6 mg/kg.Conclusions 1 .Dosage of LPS≥6 mgAg might cause ARDS in rats. 2. The remarkable upregulated AP-1 activity was associated with ALI/ARDS.
出处
《中国呼吸与危重监护杂志》
CAS
2002年第1期27-30,共4页
Chinese Journal of Respiratory and Critical Care Medicine
基金
国家自然科学基金(39730210)
全军"十五"重点课题(01Z074)
关键词
急性肺损伤
急性呼吸窘迫综合征
脂多糖
激活蛋白-1
Acute lung injury
Acute respiratory distress syndrome
Lipopolysaccharides
Activator protein-1
