摘要
本文探讨了在油酸 内毒素 (OA +LPS)介导的大鼠急性肺损伤 (ALI)模型肺组织中 ,转录因子AP 1活性变化的意义。采用OA +LPS序贯性两次致伤 ,复制ALI大鼠模型 ;采用凝胶迁移率分析法 (EMSA)检测肺组织AP 1活性。结果显示 :OA +LPS模型组大鼠呼吸窘迫 ,PaO2 早期低于 8kPa ,死亡率升高 ,肺含水量显著增加 ,肺水肿、浸润等病变严重 ,伴透明膜形成 ,肺组织AP 1活性显著升高 ;并且 ,间隔 4h两次致伤后 ,PaO2 降低幅度最大 ,死亡率高达 78.57% ,肺含水量最大 ,肺病理改变最重 ,肺组织AP 1活性最高。结果表明 :OA +LPS序贯性两次致伤 ,可以介导大鼠发生严重的ALI;ALI的发生、发展与AP
Objective:To investigate the AP 1 activity in lung of rats with acute lung injury(ALI) induced by olic acid(OA)and lipopolysaccharide(LPS).Wistar rats were injured with OA(0.2ml/kg)and LPS(2mg/kg)to set up the ALI model.Electrophoretic mobility shift assays(EMSAs)were used to measure the AP 1 activity in lung of rats.Results showed that the ALI was stimulated in rats with OA+LPS, OA+LPS might cause the significant increase the AP 1 activity in lung of rats,especially in OA+LPS/4h group.Conclusion:1.OA+LPS may cause ALI in rats.2.The initiation and development of ALI may be explained by the obvious increase of AP 1 activity.
出处
《基础医学与临床》
CSCD
北大核心
2002年第1期70-73,共4页
Basic and Clinical Medicine
基金
国家自然科学基金 (39730 2 1 0 )
