NF-κB活性对重症急性胰腺炎中腹腔巨噬细胞功能的影响  

Effect of nuclear factor-κB activation on peritoneal macrophages in rats with severe acute pancreatitis

作　　者：马振华[1] 马清涌[1] 王连才[1] 沙焕臣[1] 张梅[1] 

机构地区：[1]西安交通大学医学院第一附属医院肝胆外科,陕西西安710061

出　　处：《第四军医大学学报》2009年第13期1177-1179,共3页Journal of the Fourth Military Medical University

基　　金：教育部博士点基金青年教师项目(20070698070)

摘　　要：目的:探讨在大鼠重症急性胰腺炎(SAP)发病中腹腔巨噬细胞(PMA)炎症介质产生和释放的机制.方法:36只SD大鼠随机分为假手术组和SAP组.通过逆行胰管注射40g/L牛黄胆酸钠建立大鼠SAP模型.分别在3,6,12h剖杀大鼠.常规分离PMA并培养24h,通过凝胶电泳迁移分析法检测PMA中核转录因子-κB(NF-κB)的活性,采用酶联免疫吸附法检测细胞培养液及血清中肿瘤坏死因子-α(TNF-α)和白介素-1β(IL-1β)的水平.组间差异采用单因素方差分析进行统计学分析,P<0.05为具有显著性差异.结果:建模后3,6,12h时,NF-κB活性假手术组为6.26±0.79,7.01±0.49,6.79±0.94;SAP组为11.94±1.33,23.23±1.22,32.97±1.81.SAP组PMA细胞培养液及血清中TNF-α,IL-1β水平与NF-κB活性变化一致.在各时间点,SAP组PMA中NF-κB活性,细胞培养液及血清中TNF-α,IL-1β水平均高于假手术组(P<0.01).结论:NF-κB可以启动PMA中炎症介质的产生和释放,从而参与SAP的发生和发展.AIM： To investigate the effect of nuclear factor-κB （NF-κB） activation from peritoneal macrophages （PMA） on the production and release of inflammatory mediators in rats with severe acute pancreatitis （ SAP ）. METHODS ： Thirty-six Sprague-Dawley rats were randomly divided into control group and SAP group. To induce severe acute pancreatitis model, 40 g/L sodium taurocholate was injected into the pancreatic duct of rats through retrograde exposure of pancreatic duct in hepatic porta. Rats（n = 6, each） were sacrificed respectively at 3, 6 or 12 h after modeling. PMAs were extracted and incubated for 24 h in a humidified 5% carbon dioxide incubator. NF-κB activation in PMA was measured with electrophoretic mobility shift assay. The levels of tumor necrosis factor-α（TNF-α） and interleukin-1β （ IL- 1 β） in culture medium and serum were evaluated using ELISA method. RESULTS： NF-κB activation in control group was 6.26±0.79, 7.01 ±0.49 and 6.79 ±0.94 at 3, 6 and 12 h after modeling. NF-κB activation in SAP group was 11. 94 ± 1.33, 23.23 ± 1.22 and 32.97 ± 1.81 at each time point（P 〈 0.01 ）. The concentrations of TNF-αand IL-1β in culture medium and serum were significantly elevated in SAP group, compared with those in control group（P 〈 0. 01 ）. CONCLUSION： NF-κB activation induces the production and the release of inflammatory mediators in PMA and SAP is related to PMA activation. The inhibition of NF-κB activation may be a promising way to treat severe acute pancreatitis.

关 键 词：急性胰腺炎 腹膜巨噬细胞 核转录因子-ΚB 炎症介导素类 

分 类 号：R576[医药卫生—消化系统]