摘要
AIM： To investigate the role of nuclear factor kappa B （NF-κB） in the pathogenesis of lung injury induced by intestinal ischemia/reperfusion （I/R）, and its effect on intercellular adhesion molecule-1 （ICAM-1） expression and neutrophil infiltration. METHODS： Twenty-four Wistar rats were divided randomly into control, I/R and pyrrolidine dithiocarbamate （PDTC） treatment groups, n = 8 in each. I/R group and PDTC treatment group received superior mysenteric artery （SMA） occluding for 1 h and reperfusion for 2 h. PDTC group was administrated with intraperitoneal injection of 2% 100 mg/kg PDTC 1 h before surgery. Lung histology and bronchia alveolus lung fluid （BALF） protein were assayed. Serum IL-6, lung malondialdehyde （MDA） and myeloperoxidase （MPO） as well as the expression level of NF-κB and ICAM-1 were measured.RESULTS： Lung injury induced by intestinal I/R, was characterized by edema, hemorrhage and neutrophil infiltration as well as by the significant rising of BALF protein. Compared to control group, the levels of serum IL-6 and lung MDA and MPO increased significantly in I/R group （P=0.001）. Strong positive expression of NF-κB p65 and ICAM-1 was observed. After the administration of PDTC, the level of serum IL-6, lung MDA and MPO as well as NF-κB and ICAM-1 decreased significantly （P〈 0.05） when compared to I/R group.CONCLUSION： The activation of NF-κB plays an important role in the pathogenesis of lung injury induced by intestinal I/R through upregulating the neutrophil infiltration and lung ICAM-1 expression. PDTC as an inhibitor of NF-κB can prevent lung injury induced by intestinal I/R through inhibiting the activity of NF-κB.
瞄准：为了在肺损害的致病调查原子因素 kappa B (NF-kappaB ) 的角色，导致了旁边肠的 ischemia/reperfusion (I/R ) ，和它细胞间的粘附 molecule-1 (ICAM-1 ) 上的效果表示和嗜中性的渗入。方法：24 只 Wistar 老鼠随机被划分成控制， I/R 和吡咯烷 dithiocarbamate (PDTC ) 处理组，在各个的 n=8。I/R 组和 PDTC 治疗组织为 2 h 为 1 h 和灌注堵塞的收到的优异 mys 伤寒动脉(SMA ) 。PDTC 组在外科前与 2% 100 mg/kg PDTC 1 h 的腹膜内注射被管理。肺组织学和支气管 alveolus 肺液体(BALF ) 蛋白质是 assayed。浆液 IL-6，肺 malondialdehyde (MDA ) 和象 NF-kappaB 和 ICAM-1 的表示水平一样的 myeloperoxidase (军邮局) 被测量。结果：肺损害由肠的 I/R 导致了，被浮肿，出血和嗜中性的渗入以及由 BALF 的重要升起描绘蛋白质。比作控制组，在 I/R 显著地增加的浆液 IL-6 和肺 MDA 和军邮局的层次组织(P=0.001 ) 。NF-kappaB p65 和 ICAM-1 的强壮的积极表示被观察。在 PDTC 的管理以后，象 NF-kappaB 和 ICAM-1 一样的浆液 IL-6，肺 MDA 和军邮局的水平显著地减少了(P<0.05 ) 什么时候与 I/R 相比组。结论：NF-kappaB 的激活在肠的 I/R 直在调整嗜中性的渗入和肺 ICAM-1 表示上面导致的肺损害的致病起一个重要作用。NF-kappaB 的一个禁止者能阻止肺损害的 PDTC 通过禁止 NF-kappaB 的活动由肠的 I/R 导致了。
基金
Supported by The Natural Science Foundation of Liaoning Province,No.20042135
