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瘦素在兔急性肺血栓栓塞症并发肺损伤中的作用机制

发布时间:2018-11-21 10:55
【摘要】:目的:通过制备兔急性肺血栓栓塞症(APTE)模型,(1)观察APTE后TNF-α、IL-4和工L-1β的水平的变化。(2)给予外源性瘦素干预,观察外源性瘦素对兔APTE后TNF-a、IL-1β及超敏C反应蛋白(Hs-CRP)水平的影响,探讨炎症因子与肺损伤的关系以及如何调控对肺损伤起到保护作用。方法:选取健康新西兰兔30只,随机分为三组:对照组(同样行颈内静脉穿刺),模型组分生理盐水(NS)对照组及瘦素预处理组。用ELISA方法检测血清,术毕行病理分析。结果:1、栓塞后工L-4在发病早期未见升高,而在发病后6h明显升高,TNF-α及IL-1β水平明显高于对照组。2、形态学观察,栓塞后肺动脉内血栓形成,组织萎缩、出血及炎性反应明显。3、瘦素预处理组,TNF-α、IL-1β、Hs-CRP水平明显下降;生理盐水模型对照组明显升高于健康对照组。4、病理所见瘦素干预组缺血渗出明显轻于模型对照组。结论:1、急性肺血栓栓塞症后炎症因子发生的不同变化,在引起急性肺损伤中起重要作用。2、瘦素通过对急性肺血栓栓塞症后炎性因子TNF-α、IL-1β和Hs-CRP的水平调控,从而对肺损伤起到了保护作用。
[Abstract]:Objective: to establish (APTE) model of acute pulmonary thromboembolism in rabbits, (1) to observe the changes of TNF- 伪, IL-4 and L -1 尾 after APTE. (2) to observe the effect of exogenous leptin on TNF-a, after APTE. The effects of IL-1 尾 and high sensitive C-reactive protein (Hs-CRP) on the levels of inflammatory factors and lung injury were studied. Methods: thirty healthy New Zealand rabbits were randomly divided into three groups: control group (same as internal jugular vein puncture), model group of normal saline (NS) control group and leptin pretreatment group. ELISA method was used to detect serum and pathological analysis was performed. Results: 1. After embolization, L-4 did not increase at the early stage of embolism, but increased significantly at 6 h after embolization. The levels of TNF- 伪 and IL-1 尾 were significantly higher than those in the control group. The levels of TNF- 伪, IL-1 尾 and Hs-CRP were significantly decreased in leptin preconditioning group. The level of ischemia exudation in the model control group was significantly lower than that in the model control group, and that in the leptin intervention group was significantly less than that in the model control group. Conclusion: 1. The different changes of inflammatory factors after acute pulmonary thromboembolism play an important role in acute lung injury. 2. Leptin plays an important role in the treatment of inflammatory factor TNF- 伪 after acute pulmonary thromboembolism. The level of IL-1 尾 and Hs-CRP is regulated, which protects against lung injury.
【学位授予单位】:桂林医学院
【学位级别】:硕士
【学位授予年份】:2012
【分类号】:R563.5

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