脂多糖通过补体途径诱导小鼠产生白三烯B4  

Lipopolysaccharide Activates Serum Complement and Induces Leukotriene B4 Production in Mouse

作　　者：高婷[1] 陈婷[1] 张春梅[1] 刘萱[1] 曹诚[1] 

机构地区：[1]军事医学科学院生物工程研究所,北京100850

出　　处：《生物技术通讯》2011年第6期755-758,共4页Letters in Biotechnology

摘　　要：目的:研究脂多糖(LPS)对人血清中补体系统的激活及在小鼠模型中诱导产生白三烯B4(LTB4)。方法:LPS包被ELISA板,利用血清中补体C4、C3沉积实验检测补体成分被LPS活化的情况,通过尾静脉注射小鼠LPS后不同时间点ELISA定量检测LTB4,评价补体系统的活化和炎症因子的产生。结果与结论:血清系统ELISA检测发现LPS可以激活补体系统,且以凝集素途径为主;动物实验中LTB4被LPS诱导后1～3 h达到峰值,之后回落。C1INH对血清补体活化和动物模型中LTB4的产生均有显著抑制。Objective： To study serum complement activation by lipopolysaccharide（LPS） in human serum and the temporal distribution of leukotriene B4（LTB4） production in LPS-induced mouse model.Methods： Functional activity of the serum complement was assessed by complement C4,C3 deposition assay using immobilized LPS as a ligand.The activation of complement and the production of inflammatory factor induced by LPS in mice were investigated by ELISA for LTB4 quantitative determination at different time points.Results Conclusion： Serum complement deposition showed that LPS could induce complement activation and lectin pathway played a main role in the in vitro human serum system.In mouse model,the output of LTB4 reached its maximum during 1～3 h after injection of LPS,and then fell back,and C1INH showed inflammation inhibitory activity in both in vitro human serum system and mouse model.

关 键 词：脂多糖 补体 凝集素途径 白三烯B4 

分 类 号：R392.1[医药卫生—免疫学] Q23[医药卫生—基础医学]