胸腺肽β4提高内毒素休克小鼠存活率并下调炎症介质释放  

Thymosin β_4 raises survival rate and down-regulatesinflammatory mediators in septic shock mice

作　　者：赵裕光[1] 时德[1] 王爽[2] 

机构地区：[1]重庆医科大学临床学院普外科 [2]重庆医科大学临床学院神经内科,重庆400016

出　　处：《重庆医科大学学报》2005年第3期376-378,共3页Journal of Chongqing Medical University

摘　　要：目的:研究胸腺肽β4(thymosinβ4,Tβ4)对内毒素休克小鼠72h存活率的影响,检测TNF-α及IL-1α变化,初步探讨Tβ4治疗内毒素休克的机制。方法:选用清洁级昆明小鼠腹腔注射脂多糖(LPS)制备内毒素休克动物模型,①观察内毒素休克前后Tβ4变化情况。②Tβ4对内毒素休克小鼠存活率的影响。动物随机分为4组,每组30只,均腹腔注射LPS(25mg/kg),Ⅰ组为LPS对照组,Ⅱ、Ⅲ、Ⅳ组分别于LPS腹腔注射后0h;0h、2h;0h、2h、4h尾静脉注射Tβ4(5mg/kg),观察72h存活率。③ELISA法检测Tβ4对内毒素休克小鼠血浆TNF-α及IL-1α变化情况。结果:Tβ4在内毒素休克小鼠的血浆中明显降低,Tβ4可提高内毒素休克小鼠72h存活率,并下调TNF-α及IL-1α的释放。结论:Tβ4治疗内毒素休克应在LPS腹腔注射后0h、2h、4h连续注射Tβ4(5mg/kg),实验提示Tβ4可能是通过下调炎症介质的释放来治疗内毒素休克的。Objective:To explore the mechanism of action of thymosin β 4 (Tβ 4) in septic shock by observing the 72h survival rate of septic shock mice treated with thymosin β 4 and exploring the changes of TNF-α and IL-1α.Methods:LPS(lipopolysaccharide) was intraperitoneally injected into clean Kunming mice to establish the animal model.①The Tβ 4,between normal and septic shock mice were determined.②The survival rate of septic shock mice was studied by intraperitoneal injection of Tβ 4.Animals were divided into four groups of 30 and each received LPS(25mg/kg)intraperitoneal injection.Group Ⅰ was LPS control group.GroupⅡ,Ⅲ and Ⅳ were individually injected with Tβ 4 at 0h,0h,2h;0h,2h,4h post LPS through caudal vein.③TNF-α and IL-1α were examined in septic shock mice by ELISA.Results:Tβ 4 was obviously decreased in the blood of septic shock mice.Tβ 4 could raise the 72h survival rate of septic shock mice and down-regulate inflammatory mediators.Conclusion:The optimal protective methods in the mouse appears to be 5mg/kg Tβ 4 given immediately following(0h) and at 2h and 4h successively post LPS.Tβ 4 down-regulates the inflammatory mediators,which may be the mechanism of Tβ 4 in curing the septic shock.

关 键 词：胸腺肽β4 存活率 TNF—α IL—1α 

分 类 号：R363[医药卫生—病理学]