摘要
目的探讨核转录因子-kappaB（NF-κB）在急性重症胰腺炎肺损伤发病中的作用及不同药物的影响。方法经胆胰管逆行注射去氧胆酸钠复制大鼠急性重症胰腺炎肺损伤模型。采用凝胶电泳迁移率改变。（EMSA）法检测肺泡巨噬细胞中NF-κB活性,同时应用逆转录-聚合酶链式反应（RT-PCR）检测肺泡巨噬细胞中诱生性一氧化氮合酶基因（iNOS mRNA）的表达情况,并检测一氧化氮（NO）、肿瘤坏死因子α（TNF-α）、诱生型一氧化氮合酶（iNOS）的含量和肺组织病理学改变。结果模型组NF-κB活性增强、iNOS mRNA出现高表达,相应的TNF-a、NO、iNOS均明显高于假手术组。地塞米松和善宁可以下调NF-κB活性,减少iNOS mRNA表达,减轻肺损伤程度,而凯复定则无明显作用。结论急性重症胰腺炎肺损伤时,NF-κB活化,进而启动TNF-α、iNOS、NO大量表达,在发病中起着十分重要的作用。地塞米松和善宁可以通过调节NF-κB活化等多种途径,防止肺组织的进一步损害。
Objective To investigate the effects of nuclear factor-κB （NF-κB） activation in acute lung injury（ALI） induced by acute severe pancreatitis（ASP） and the regulatory effects of different drugs.Method The ALI models in the rats were produced by retrograde injection of deoxysodium cholate into the bilipancreatic duct.NF-κB activity and iNOS mRNA in alveoli macrophage were determined by electrophoretic mobility gel shift assay （EMSA） and reverse transcription polymerasechain reaction （RT-PCR）,respectively. The levels of NO, TNF-α, iNOS and pathological changes were determined. Results NF-κB activity was strengthened, iNOS mRNA expression was increased, and levels of TNF-α, NO and iNOS in model group were significantly higher than those in sham operation control group. Dexamethasone and sandostatin down-regulated the activity of NF-κB and reduced expression of iNOS mRNA, and alleviated the lung injury. But Kefadin had no obvious effects. Conclusions In ALI rats induced by ASP, NF-κB was activated, NF-κB caused the over-expression of TNF-α, iNOS and NO, which was very important in the course of ALI. Dexamethasone and sandostatin could alleviate lung injury through rgulating NF-κB.
出处
《中华急诊医学杂志》
CAS
CSCD
2007年第4期373-377,共5页
Chinese Journal of Emergency Medicine
基金
国家自然科学基金资助项目（30271667）.
