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- W3032459651 abstract "目的本研究旨在动态观察急性坏死性胰腺炎(ANP)大鼠肠黏膜核因子κB(NFκB)及其介导的细胞因子,包括肿瘤坏死因子α(TNFα)、白介素1(IL-1β)、诱导型一氧化氮合成酶(iNOS)、细胞间黏附分子(ICAM-1)和单核细胞趋化蛋白(MCP-1)mRNA的变化,探讨其在ANP并发肠道衰竭发生中的作用;并观察生长激素(GH)对NFκB活化及细胞因子表达的下调作用.方法SD大鼠72只,随机分为三组:假手术组(SO);ANP组;ANP+GH组.GH治疗组术后皮下注射GH溶液(0.75 U/kg体重),非治疗组则注射等容积生理盐水作对照.大鼠胆胰管内逆行注射5%牛磺胆酸钠溶液制备ANP模型.提取肠组织RNA,逆转录聚合酶链反应(RT-PCR)研究术后6,12,24 h肠黏膜TNFα、IL-1β、iNOS、ICAM-1、MCP-1 mRNA表达.术后3,6,12,24 h免疫组化法检测肠黏膜NFκB的活化情况.结果ANP组大鼠肠黏膜TNFα、IL-1β、iNOS、ICAM-1和MCP-1 mRNA表达较SO组增高,其中TNFα和IL-1β mRNA表达于术后6 h达峰值,且较SO组差异显著(TNFα:1.03±0.17 vs 0.34±0.07;IL-1β:0.91±0.08 vs 0.39±0.06,P＜0.05);iNOS和ICAM-1 mRNA表达于术后12 h达峰值,较SO组差异显著(iNOS:0.62±0.10 vs 0.04±0.02;ICAM-1:1.48±0.33 vs 0.21±0.15,P＜0.05);MCP-1 mRNA表达随时间延长而升高(0.20±0.05;0.23±0.02;0.31±0.04),较SO组(0.13±0.01;0.11±0.01;0.09±0.02)增高显著,P＜0.05.GH治疗组TNFα、IL-1β、iN-OS、ICAM-1和MCP-1 mRNA表达均显著下调,P＜0.05.SO组大鼠肠黏膜鲜见NFκB活化的细胞,而ANP组大鼠术后3 h肠黏膜即出现大量核内NFκB p65亚单位染色阳性细胞,主要分布于肠绒毛顶端.GH治疗组肠黏膜NFκB活化细胞明显少于ANP组.结论NFκB活化及其介导的细胞因子过度表达参与了ANP大鼠肠黏膜损伤.GH能显著降低ANP肠黏膜组织炎性细胞因子、黏附分子和趋化蛋白的转录,从而发挥其肠道局部抗炎效应,此作用与其抑制NFκB活化有关." @default.
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- W3032459651 date "2003-01-28" @default.
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- W3032459651 title "Nuclear factor κB-mediated cytokines over-expression in intestinal mucosa of acute necrotizing pancreatitis and influence of growth factor in rats" @default.
- W3032459651 doi "https://doi.org/10.3760/cma.j.issn.1007-8118.2003.01.015" @default.
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