内毒素致兔ARDS模型IL-23和IL-27的变化及血必净的干预作用

摘要

Objective To investigate the mechanism of acute respiratory distress syndrome (ARDS) by measuring the changes of interleukin-23 (IL-23),IL-27,plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (t-PA) in ARDS rabbit models.Methods 24 male Japanese flap eared white rabbits were randomly divided into three groups:control group (group A),endotoxin induced ARDS group (group B) and Xuebijing treatment group (group C).ARDS rabbit models were replicated by intravenous injection of endotoxin (750 μg/kg) in group B and group C,and Xuebijing (1.8 ml /kg)was administered intravenously in group C.IL-23,IL-27,PAI-1 and t-PA were measured.Results Compared with group A,the expression of IL 23 was increased and IL-27 was decreased in group B (P ＜0.05 or P ＜0.01).The level of IL-23 in group C was also increased than that in group A,but it was lower than that in group B (P ＜0.05 orP ＜0.01).The level of IL-27 in group C was lower than that in group A and group B (P ＜0.05 or P ＜0.01).The level of t-PA in group B was significantly higher than that in group A (P ＜0.01).There was no significant difference in the level of t-PA between group A and group C.The level of PAI-1 in group B was higher than that in group A (P ＜0.01) and group C (P ＜0.05 or P ＜0.01).The level of PAI-1 in group C was higher than that in group A (P ＜0.01).Conclusions ARDS has imbalance of inflammatory reaction,imbalance between proinflammatory and antiinflammatory reactions.Coagulation-fibrinolysis is abnormal,procoagulation and anticoagulation is imbalanced after injury induced by endotoxin.Xuebijing can antagonize the release of inflammatory mediators caused by endotoxin and improve the abnormal coagulation mechanism.%目的 通过观察兔急性呼吸窘迫综合征(ARDS)模型白介素23(IL-23)、IL-27及纤溶酶原激活剂抑制物1(PAI-1)、组织纤溶酶原激活剂(t-PA)的变化,探讨内毒素致伤机制,旨在为临床防治ARDS提供理论参考.方法 将24只日本大耳白兔随机分为对照组、内毒素致伤组及血必净干预组.用内毒素(750 μg/kg)一次性静脉注射方法复制兔ARDS模型,应用血必净按1.8 ml/kg静脉注射进行干预,分别检测血液中IL-23、IL-27及PAI-1、t-PA的变化.结果 内毒素致伤组实验后各时间点IL-23均高于对照组(P＜0.05或P＜0.01),1h时下降明显,2h有上升趋势.血必净干预组IL-23水平始终低于内毒素致伤组(P＜0.05或P＜0.01),在实验后1h时有一较大幅度的下降.内毒素致伤组IL-27在实验后各时间点低于对照组(P＜0.05或P＜0.01),1h时同样有明显下降,至4h虽有上升趋势但始终低于对照组.血必净干预组IL-27明显低于对照组、内毒素致伤组(P ＜0.05或P＜0.01).内毒素致伤组实验后t-PA升高(P＜0.01),并且在1h时升高幅度较大,随着时间的延长其含量呈下降趋势,但始终高于对照组.血必净干预组t-PA与对照组比较差异无统计学意义.内毒素致伤组血浆PAI-1水平在静脉注射内毒素后高于对照组(P＜0.01),血必净干预组PAI-1较对照组升高(P＜0.01),但低于内毒素致伤组(P＜0.05或P＜0.01).结论 ARDS存在炎症反应失控,促炎反应和抗炎反应平衡失调.内毒素致伤后凝血纤溶异常,促凝和抗凝失衡.血必净可以拮抗内毒素引起的炎症介质释放失控,改善凝血机制异常.