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目的探讨核因子-κB(NF-κB)抑制剂氟美松对大鼠供肺缺血-再灌注损伤的保护作用。方法24只大鼠随机分为两组,实验组采用含氟美松的低钾右旋糖酐(LPD)液灌洗和保存供肺,对照组以LPD液灌洗和保存供肺,16h后建立离体肺再灌注模型,循环灌注1h。再灌注期间,每隔15min测定供肺氧合后动脉血氧分压(PaO2)和气道峰压(PawP);再灌注结束后测定肺组织湿重与干重比(W/D)以及肺组织中髓过氧化物酶(MPO)活性、细胞间粘附分子(ICAM-1)和NF-κB的表达。结果再灌注15min后,两个组的PaO2逐渐降低、PawP逐渐升高,但实验组PaO2的降低程度和PawP的升高程度明显低于对照组(P<0.01);再灌注后,实验组的W/D和MPO明显低于对照组(P<0.01),其肺组织中ICAM-1、ICAM-1mRNA、NF-κB及NF-κBmRNA的表达量也明显低于对照组(P<0.01)。结论应用氟美松抑制NF-κB的表达对大鼠供肺缺血-再灌注损伤具有保护作用。
Objective To investigate the protective effect of dexamethasone, an inhibitor of nuclear factor-κB (NF-κB), on lung ischemia-reperfusion injury in rats. Methods Twenty-four rats were randomly divided into two groups. The experimental group was treated with LPD solution containing flumethasone for lung preservation. The control group was lavaged with LPD fluid and preserved for lung. After 16 hours, Lung reperfusion model, perfusion 1h. During reperfusion, arterial oxygenation (PaO2) and airway pressure (PawP) were measured every 15 minutes after reoxygenation. The ratio of wet to dry weight (W / D) and lung tissue Myeloperoxidase (MPO) activity, intercellular adhesion molecule (ICAM-1) and NF-κB expression. Results After reperfusion for 15 minutes, PaO2 decreased gradually and PawP increased gradually in both groups, but the decrease of PaO2 and the increase of PawP in experimental group were significantly lower than those in control group (P <0.01). After reperfusion, W / D and MPO were significantly lower than those in the control group (P <0.01). The expression of ICAM-1, ICAM-1mRNA, NF-κB and NF-κB in the lung tissue were also significantly lower than those in the control group (P <0.01). Conclusion The use of flumethasone to inhibit the expression of NF-κB has a protective effect on pulmonary ischemia-reperfusion injury in rats.