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作 者:滕晓丽[1] 赵秋[1] 杜静[1] 谷华[1] 覃华[1]
机构地区:[1]华中科技大学同济医学院附属同济医院消化内科,湖北省武汉市430030
出 处:《世界华人消化杂志》2006年第4期438-441,共4页World Chinese Journal of Digestology
摘 要:目的:观察重症急性胰腺炎(SAP)大鼠白血病抑制因子(LIF)在肺组织中表达的时相变化, 探讨LIF在SAP病程及肺损伤中的意义.方法:36只♂SD大鼠随机分为正常对照组(N 组,n=6)、假手术组(Sham组,n=6)和重症急性胰腺炎组(SAP组,n=24).采用胰管逆行灌注50 g/L牛磺胆酸钠的方法复制大鼠SAP模型.用RT-PCR法检测肺组织中LIF mRNA的表达水平,免疫组织化学方法检测NLIF在肺组织中的表达变化.结果:SAP组3 h后肺组织LIF mRNA的表达量明显高于对照组和假手术组(灰度值:1.018± 0.065 vs 1.451±0.067,1.322±0.072,P<0,05), 并且6,12,24 h持续升高(0.853±0.058,0.635 ±0.064,0.582±0.089)(P<0.01).同样,SAP组 LIF蛋白表达在3和6 h后明显高于对照组和假手术(127.36±2.76,122.53±2.43 vs 159.46 ±2.78,156.35±3.12,P<0.05),并且12,24 h后也维持在很高的水平(109.37±2.87,102.42± 2.27).结论:LIF作为促炎症因子参与了SAP肺组织的炎症反应.AIM: To observe the levels of leukemia inhibitory factor (LIF) in the pulmonary tissues in rats with severe acute pancreatitis (SAP), and to investigate the role of LIF in the progression of SAP and lung injury. METHODS: Thirty-six male Sprague Dawley rats were randomly divided into three groups: normal control (n = 6), sham operation (n = 6), and SAP (n = 24) group. SAP model was induced by retrograde injection of 50 g/L sodium taurocholate into the pancreatobiliary duct. The expression of pulmonary LIF mRNA was detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR), and the expression of LIF protein was detected by immunohistochemistry. RESULTS: The level of pulmonary LIF mRNA expression was increased significantly in SAP group at 3 h in comparison with that in normal control and sham operation group (grey value: 1.018 ± 0.065 vs 1.451 ± 0.067, 1.322 ± 0.072, both P 〈 0.05), and maintained at high levels up to 24 h after modeling (0.853 ± 0.058, 0.635 ± 0.064, 0.582 ± 0.089 for 6, 12, and 24 h, respectively, P 〈 0.01). Similarly, the expression of pulmonary LIF protein was also markedly increased in SAP group 3 and 6 h after modeling as compared with that in normal and sham operation group (grey value: 127.36 ± 2.76, 122.53 ± 2.43 vs 159.46 ± 2.78, 156.35 ± 3.12, all P 〈 0.05), and main- tained at high levels at 12 and 24 h (109.37 ± 2.87, 102.42 ± 2.27, respectively)(P 〈 0.01). CONCLUSION: LIF acts as a proinflammatory mediator in SAP.
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