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机构地区:[1]广东医学院附属医院消化科,广东湛江524001 [2]广东药学院门诊部,广东广州510224
出 处:《南方医科大学学报》2008年第4期600-602,605,共4页Journal of Southern Medical University
基 金:广东省卫生厅课题(A2005325)
摘 要:目的探讨葡聚糖硫酸钠(DSS)诱导的结肠炎小鼠NF-κB活性、ICAM-1蛋白表达变化及NF-κB对其调控作用。方法取健康雄性BABC/L小鼠20只,采用5%DSS溶液结肠炎小鼠模型和0.9%盐水溶液(NS)为正常对照组。免疫组化方法检测细胞间粘附分子(ICAM-1)和NF-κBp65表达水平,凝胶滞留迁移试验(EMSA)测定NF-κB的DNA结合活性。结果DSS组较NS组NF-κBDNA结合活性显著升高,具统计学意义(P<0.01),NF-κBp65成份主要表达于粘膜下层的炎症细胞及部分血管内皮细胞,出现核移位现象,正常对照组仅少数细胞表达p65,ICAM-1。相关性分析提示NF-κB活性与ICAM-1表达呈正相关性。结论DSS诱导结肠炎小鼠结肠粘膜的NF-κB明显活化,可能上调了ICAM-1基因的表达,参与肠道炎症的发生发展。Objective To investigate the changes in the activity of nuclear factor-kB (NF-kB) in mice with dextran sulphate sodium (DSS)-induced rat colitis and its modulalorg effect on intercellular adhesion molecule-I (ICAM-I) expression. Methods Twenty normal male mice were randomized into DSS group and normal saline (NS) control group according to a matched-pair design. From days 1 to 7, the mice in DSS group were subjected to oral administration of 5%DSS solution, and from days 8 to 20, NS was given instead, for a total of 3 cycles. In the control group, only NS was administered. The colonic pathology was observed using HE staining and the mucosa 1 damage was scored for each mouse. The DNA-binding activity of NF-KB was tested by electrophoretic mobility shift assay, and the expressions of ICAM-I and NF-kB p65 were detected using immunohistochemistry. Results The DNA-binding activity of NF-kB was significantly increased in DSS group as compared with NS group. ICAM-I and p65 expressions were detected in the nuclei of the vascular endothelial and inflammatory cells, especially in the mucosa and submucosa, but such positive cells were seldom observed in NS group. A positive correlation was found between the DNA-binding activity of NF-kB and ICAM-I expression. Conclusion NF-kB activation is an important event in the development of DSS-induced colitis in that activated NF-kB upregulates ICAM-I expression during colonic inflammation.
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