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目的:探讨重症急性胰腺炎(SAP)大鼠肺组织核因子-κB(NF-κB)活化及诱导型一氧化氮合酶mRNA表达与肺损伤的关系。方法:SD大鼠随机分为对照组、SAP组、二硫代氨基甲酸吡咯烷(PDTC)预处理组。建立各组模型后取肺组织行病理学观察,免疫组织化学法观察NF-κB的表达,实时荧光定量PCR法检测iNOS mRNA表达。结果:对照组仅极少量NF-κB活化,iNOS mRNA呈低水平表达。SAP组NF-κB表达明显增加,并呈动态变化,6h达高峰,主要表达于中性粒细胞、单核/巨噬细胞、支气管黏膜上皮细胞、肺泡上皮细胞的胞质和胞核内,iNOSmRNA表达明显上调。PDTC预处理组NF-κB表达明显减少,iNOS mRNA表达亦下调,但仍高于对照组。结论:SAP时肺组织NF-κB活化并通过调控iNOS mR-NA的表达参与肺损伤。PDTC可能通过抑制NF-κB活性进而下调iNOS mRNA的表达,减轻肺损伤。
Objective: To investigate the relationship between the activation of nuclear factor-κB (NF-κB) and the expression of inducible nitric oxide synthase mRNA in lung tissue and lung injury in severe acute pancreatitis (SAP) rats. Methods: SD rats were randomly divided into control group, SAP group and pyrrolidine dithiocarbamate (PDTC) pretreatment group. Pathological examination of lung tissue was performed after establishing the model of each group. The expression of NF-κB was detected by immunohistochemical method. The expression of iNOS mRNA was detected by real-time fluorescence quantitative PCR. Results: In the control group, only a small amount of NF-κB activation, iNOS mRNA was low expression. The expression of NF-κB in SAP group increased significantly and reached a peak at 6h, which was mainly expressed in the neutrophils, monocytes / macrophages, bronchial epithelial cells, alveolar epithelial cells in the cytoplasm and nucleus, iNOS mRNA The expression was significantly increased. PDTC pretreatment group, NF-κB expression was significantly reduced, iNOS mRNA expression was down, but still higher than the control group. Conclusion: NF-κB activation in the lungs of SAP is involved in lung injury by regulating the expression of iNOS mR-NA. PDTC may reduce iNOS mRNA expression and reduce lung injury by inhibiting NF-κB activity.