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机构地区:[1]湖南省人民医院急诊科,湖南长沙410005 [2]湖南省人民医院普外科 [3]湖南省人民医院病理科
出 处:《中国医师杂志》2009年第9期1174-1177,共4页Journal of Chinese Physician
基 金:湖南省教育厅科研基金资助项目(07C573);湖南省卫生厅科研基金资助项目(B2007134);湖南省人民医院仁术重点科研基金项目(2006年)
摘 要:目的探讨维生素D受体(VDR)失活对APCmin/+小鼠肠道肿瘤生长的影响及机制。方法通过构建APCmin/+VDR-/-小鼠模型(n=8),与APCmin/+小鼠比较(n=8),4月龄时观察肠道肿瘤大小及数目情况,肿瘤作HE染色以判断病理类型。免疫组化检测肿瘤相关基因BCL-2、vimentin-1、Stat-1和MSH-2蛋白的表达。结果4月龄时2组鼠比较,APCmin/+VDR-/-小鼠〉3mm肿瘤明显增多(P〈0.01)。HE染色显示肠道肿瘤为管状腺瘤。APCmin/+肿瘤的Stat-1表达较强,而MSH-2和vimentin-1表达在APCmin/+VDR-/-肿瘤中均更强。结论维生素D受体缺失促使APCmin/+小鼠肠道肿瘤的发展。Objective To explore effects and mechanism of inactivation of vitamin D receptor (VDR) in intestinal tumor growth of APCmin/+ mice. Methods To generate APCmin/+ VDR -/- mice through breeding, the number and size of small intestinal and colonic tumors were assessed and compared between APCmin/+ and APCmin/+ VDR -/- mice. The intestinal tumors were diagnosed with HE stain. The expressions of BCL-2 ,vimentin-1 ,Stat-1 and MSH-2 proteins of tumors were determined by immunohistochemistry and compared be- tween APCmin/+ and APCmin/+ VDR - / - mice. Results A comparison between APCmin/+ and APCmin/+ VDR - / - mice revealed that the number of the tumors, which were larger than 3mm, was significantly increased in APCmin/+ VDR -/- mice at 4 months of age ( P 〈 0. 01 ). HE staining indicated fistulous adenomas from small intestine and colon of two groups. Immunostaining showed Stat - 1 level in APC- rain/+ tumors were increased and MSH-2 and vimentin-1 levels in APCmin/+ VDR -/- mice were increased, compared to APCmin/+ tumors. Conclusion These observations suggested that inactivation of VDR promoted the intestinal tumor growth of APCmin/+mice.
关 键 词:肠肿瘤/遗传学 受体 骨化三醇/生物合成 基因 bcl-2/生物合成 中间丝蛋白质类/生物合成 原癌基因蛋白质类/生物合成
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