摘要
[目的]观察内毒素血症引起兔脂质过氧化产物、炎症因子水平改变,运用促红细胞生成素(EPO)进行干预。[方法]兔股动脉放血造休克随后复苏,予腹腔注射内毒素,两次打击造成兔多脏器功能不全模型;24只健康新西兰大白兔随机分成对照组、二次打击组、EPO组,每组8只;造模前后留取血标本用于检测TNFα、IL6、IL10、MDA等指标。[结果]二次打击致其它两组MDA水平明显高于对照组,EPO组MDA水平较二次打击组明显降低;二次打击致其它两组TNFα、IL6、IL10水平明显高于对照组,EPO组明显低于二次打击组。[结论]TNF-α,IL-6,IL-10等炎症因子与MDA等脂质过氧化产物参与了失血性休克合并内毒素血症所致多脏器损伤的过程,EPO能降低失血性休克合并内毒素血症兔炎症因子及脂质过氧化产物水平。
[Objective]To explore the rabbits' lipid peroxidation and cytokine level change caused by endotoxemia,use EPO for intervention.[Method]Bleed rabbits femoral for shock,after coming to,make injection of endotoxin,two beatings make dysfunctional multi-organs model;randomly divide 24 healthy rabbits into control group(1),2-beating group(2),EPO group(3),8 in each;take blood for testing indexes of TNFα,IL6,IL10 and MDA.[Result]Group 2 was higher than other groups on MDA level,group 3 less than group 2;group 2 was much higher than other 2 groups on TNFα,IL6 and IL10,group 3 less than group 2.[Conclusion]The cytokines and lipid peroxidation participating in the course of multi-organ injury caused by blood loss shock and endotoxemia can be reduced by EPO.
出处
《浙江中医药大学学报》
CAS
2010年第2期155-157,共3页
Journal of Zhejiang Chinese Medical University