中文摘要：

观察急性坏死性胰腺炎（ANP）大鼠肠粘膜绒毛细胞（IMN）核因子KB（NF—kB）及其介导的细胞因子的变化，探讨其在ANP并发肠道衰竭中所起的作用，并观察生长激素（GH）对NF—kB活化及细胞因子的下调作用。方法：36只SD大鼠随机分成正常对照组，ANP组，GH处理组。采用5％牛磺胆酸钠逆行性胰胆管注射制备ANP动物模型，GH处理组在造模前30min经尾静脉注射GH（0．75U／kg）。术后6h处死各组动物，行末端回肠灌洗，检测末端回肠灌洗液（TILF）中TNF—α、IL-1β、iNOS、ICAM-1和MCP-1含量，检测肠粘膜细胞中NF—KB活性水平，并行肠粘膜组织病理学检查。结果：对照组末端回肠组织未见病理改变，ANP组和GH处理组末端回肠组织均出现充血、水肿、炎性渗出等病理改变，但GH处理组病变程度轻与ANP组；ANP组TILF的TNF-α、IL-1β、iNOS、ICAM-1和MCP-1含量较正常对照组明显升高。GH处理组肠粘膜NF—KB活化细胞明显少于ANP组；ANP组，GH处理组IMN中NF—KB的表达活性呈负相关。结论：NF—kB活化及其介导的细胞因子过度表达参与了ANP大鼠肠粘膜损伤，GH能显著降低肠粘膜组织炎性细胞因子、粘附分子和趋化蛋白的表达，减少NF-kB活化，进而减轻肠粘膜损伤。

英文摘要：

Objective：To investigate the unclear factor kB（NF-kB） and NFkB mediated cytokines ove-exper ession in the cells of intestinal mucoasal nap（IMN） on intestinal failure during acute necrotizing pancreatitis （ANP） and the down-regulation of growth hormone （GH） upon them. Methods：Thirty-six SD rates were equally randomized into the nor mal control group, ANP group and GH pretreatment group. The ANP model was established by retrograde injection of 5 % sodium taurocholate into the biliopanereatic duct and the GH pretreatment group were injected with GH （0. 75U/kg ） through tail vein 30min prior to model establishment. Animals were sacrificed 6h after ANP induction, and then the IMN were harvested via terminal ileum mucosa fluff lavage. The contents of TNF- a , IL- lβ,iNOS,ICAM-1 and MCP1 in terminal ileum lavage fluid（TILF） were detected,and the activation levels of NF-kB in IMN were determined by Western blot analysis. The terminal ileum tissues were measured and pathological examination of the terminal ileum tissues was performed. Results： No pathological change was found in terminal ileum tissues of the normal control group, while the terminal ileum tissues of both the ANP and GH pretreatment group showed marked pathological changes such as congestion, edema and accumulation of inflammatory exudates, but these changes of the GH pretreatment group were relatively mild compared with the ANP group. The contents of TNF- α , IL- Iβ,iNOS, ICAM-1 and MCP-1 in the TILF were all significantly in creased in the ANP group compared with the normal control group. The degree of NF-~B activation was decreased in GH pretreatment group as compared with ANP group. There were negative correlations the expression of NF-kB in the IMN of the ANP group and GH pretreatment group. Conclusion： Activation of NF-kB and NF-kB mediated cytokine expression is one of the major factor for intestinal failure in ANP. The GH can significantly reduce expression on the intestinal mucosa tis sue inflammatory cells facto