急性坏死性胰腺炎肺组织炎性介质mRNA表达与肺损伤的关系

摘要

目的 探讨急性坏死性胰腺炎(ANP)大鼠肺组织白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)及细胞间黏附分子(ICAM-1)等炎性介质mRNA表达与肺损伤的关系.方法 33只Wistar大鼠随机分为正常对照和胰腺炎不同时间点(1、4、12和24 h)各组,应用3.5%牛磺胆酸钠逆行胰胆管注射制备ANP模型.采用RT-PCR法检测ANP肺组织IL-6、TNF-α及ICAM-1 mRNA表达,同时观察血淀粉酶及脂肪酶、胰腺和肺组织湿/干重比率及病理改变.结果 造模ANP 1 h后肺组织IL-6、TNF-α及ICAM-1 mRNA水平(1.25±0.16、0.33±0.09及082±0.03)较正常对照组(0.07±0.02、0.06±0.02及0.41±0.04)表达增高(P<0.05),并持续升高至12及24 h(分别为1.674±0.14、0.99±0.11、1.17士0.05及1.87±0.05、0.96士0.06、1.11士0.04),同时伴有肺组织病理损害,其严重程度与肺TNF-α及ICAM-1 mRNA表达、肺组织湿/干重比率与TNF-α、IL-6、ICAM-1 mRNA表达的相关系数分别为0.93及0.70(P<0.05).结论 大鼠ANP早期肺组织IL-6、TNF-α及ICAM-1mRNA即过度表达,肺IL-6、TNF-α及ICAM-1mRNA过度表达是ANP肺损害发生的原因之一,肺损伤严重程度与IL-6、TNF-α及ICAM-1mRNA表达的高低有关.%Objective To investigate intrapulmonary expression of IL-6,TNF-α and intercellular adhesion molecule-1 (ICAM-1) mRNA and relationship between the gene expression of inflammatory mediators and lung injury in acute necrotizing pancreatitis (ANP). Methods ANP was induced with 3.5% sodium taurocholate by the method of retrograde pancreatic-injection. Animals were sacrificed at 1, 4, 12 and 24 hours after induction of pancreatitis, lntrapulmonary IL-6, TNF-α and ICAM-1 and mR-NA expression was assayed by reverse transcription-PCR. The serum amylases and lipases levels,pancreatic and pulmonary wet/dry weight ratio, histologic grading of ANP and lung injury were deter-mined. Results Taurocholate pancreatitis showed alveolar septal thickening and leucocyte infiltration in the lung. There was intrapulmonary overexpression of the IL-6,TNF-α and ICAM-1 mRNA at 1hour and persisted up to 12-24 hours with the increase of serum amylases and lipases levels after induc-tion of pancreatitis. Score of the lung injury was correlated well with expression of TNF-a and ICAM-1 mRNA (r=0.93, P<0.05). Pulmonary wet/dry weight ratio was correlated with intrapulmonary expression of the IL-6, TNF-α and ICAM-1 mRNA (r=0.70,P<0.05). Conclusion The expression of IL-6, TNF-u and ICAM-lmRNA is related to the production of lung injury in ANP. Severity of lung injury can be early assessed by the overexpression of IL-6, TNF-α and ICAM-lmRNA in ANP.