大鼠肺组织深低温缺血再灌注后AQP-5、NF-κB、TNF-α含量变化与肺损伤的关系

发布时间：2018-04-09 21:38

本文选题：深低温缺血再灌注　切入点：急性肺损伤　出处：《武汉大学学报(医学版)》2014年02期

【摘要】：目的:探讨深低温缺血再灌注后肺组织水通道蛋白5(AQP-5)、核转录因子κB(NF-κB)、肿瘤坏死因子α(TNF-α)的变化及其与肺损伤之间的关系。方法:40只Wistar大鼠随机分为实验组16只(Z组)、对照组16只(D组)和正常组8只。实验组大鼠体表降温至深低温后阻断左下肺门,分别于阻断前、阻断后30min、60min、2h、再灌注复温后12h、24h取肺组织,对照组同时开始降温复温,但不阻断左下肺门,于对应时间点取肺组织,正常组不降温,仅于实验组阻断前开胸取相应位置肺组织,随即关胸。测量所有肺组织湿/干重(W/D)比值,病理学染色观察肺组织结构变化,用Western blot方法检测肺组织AQP-5、NF-κB、TNF-α的蛋白表达变化。结果:与正常组比较,实验组和对照组深低温后肺组织W/D比值开始上升,病理学染色提示不同程度的肺泡间质水肿与肺泡结构破坏,AQP-5、TNF-α和NF-κB蛋白表达上调,实验组于开放12h达到高峰(与正常组比较P0.01);对照组AQP-5于升温24h达到高峰(与正常组比较P0.01),NF-κB和TNF-α的蛋白表达高峰出现于开放复温后12h(与正常组比较P0.01)。与对照组比较,实验组肺组织W/D比值上升与肺组织结构破坏更明显,且在深低温阻断2h至开放复温24h时间段,实验组AQP-5、TNF-α和NF-κB蛋白表达相较对照组增加更为明显(P0.05)。结论:深低温缺血再灌注造成急性肺损伤,随之TNF-α、NF-κB的表达升高,而与此同时由于内源性保护机制的启动,AQP-5的表达也随之明显升高。
[Abstract]:Aim: to investigate the changes of aquaporin 5 (AQP-5), nuclear factor 魏 B (NF- 魏 B), tumor necrosis factor 伪 (TNF- 伪) in lung tissue after deep hypothermia ischemia reperfusion and its relationship with lung injury.Methods 40 Wistar rats were randomly divided into experimental group (n = 16) and control group (n = 16) and normal group (n = 8).In the experimental group, the left lower lung hilum was blocked after deep hypothermia, and the lung tissue was removed at the same time before the occlusion, 30 minutes after the occlusion and 12 hours after rewarming. In the control group, the left lower pulmonary hilus was not blocked, and the lung tissue was taken at the corresponding time point, while the control group began to cool down and rewarming at the same time.In the normal group, the lung tissue was removed before blocking, and then closed.The wet / dry weight W / D ratios of all lung tissues were measured, the changes of lung structure were observed by pathological staining, and the protein expression of AQP-5 / NF- 魏 TNF- 伪 was detected by Western blot method.Results: compared with normal group, the ratio of W / D in lung tissue of experimental group and control group began to rise after deep hypothermia. Pathological staining indicated that the expression of TNF- 伪 and NF- 魏 B in alveolar interstitial edema and alveolar structure destruction were up-regulated.The expression of NF- 魏 B and TNF- 伪 in the experimental group reached the peak at 12 h after opening (compared with the normal group, P 0.01) and the AQP-5 in the control group reached the peak at 24 h after opening (compared with the normal group, the protein expression of NF- 魏 B and TNF- 伪 appeared at 12 h after rewarming compared with the normal group).Compared with the control group, the increase of W / D ratio in the experimental group was more obvious than that in the control group, and the expression of AQP-5 TNF- 伪 and NF- 魏 B protein in the experimental group was significantly higher than that in the control group at the time of deep hypothermia block for 2 hours and open rewarming for 24 hours.Conclusion: acute lung injury induced by deep hypothermia ischemia reperfusion leads to an increase in the expression of TNF- 伪 -NF- 魏 B, and at the same time, the expression of AQP-5 is also significantly increased due to the initiation of endogenous protective mechanism.
【作者单位】：武汉大学人民医院心血管外科;
【分类号】：R563

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