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[目的]观察结肠黏膜核苷酸结合寡聚化结构域样受体-3(NLRP-3)炎症小体、肠黏膜内趋化因子-3(CCL-3)在溃疡性结肠炎(UC)小鼠中的表达,探讨UC的可能发病机制。[方法]40只雄性Balb-c小鼠按体重随机分为正常组和模型组,应用自由饮用3%DSS连续1周法制备UC模型。1周后处死全部小鼠。采用苏木精-伊红及透射电镜检测结肠组织病理学及超微结构变化,采用荧光定量PCR及Western-blot技术检测结肠黏膜NLRP-3炎症小体、CCL-3表达变化。[结果]与正常组比较,光镜下模型组黏膜上皮脱落,黏膜层可见大量炎性细胞浸润,并溃疡形成;电镜下模型组上皮细胞微绒毛稀疏甚至脱落消失;细胞间复合连接松解消失;核固缩,细胞处于坏死期。模型组NLRP-3及CCL-3蛋白及mRNA表达呈上升趋势,分别为1.36±0.25、1.58±0.17、1.52±0.16及1.49±0.13,与正常组比较,差异有统计学意义(P<0.05)。[结论]UC存在结肠黏膜NLRP3介导CCL-3高表达变化,以NLRP-3炎症小体为治疗靶点对于UC防治将有望提供新的思路。
[Objective] To observe the effect of colon mucosa nucleotide-binding oligomeric domain-like receptor-3 (NLRP-3) inflammasome and intestinal mucosal chemokine-3 (CCL- Mice to explore the possible pathogenesis of UC. [Methods] Forty male Balb-c mice were randomly divided into normal group and model group according to body weight. UC models were prepared by freely drinking 3% DSS for 1 week. All mice were sacrificed after 1 week. The histopathological and ultrastructural changes of colonic tissue were detected by hematoxylin-eosin and transmission electron microscopy. The expression of CCL-3 in NLRP-3 inflammasome and colonic mucosa were detected by real-time PCR and Western-blot. [Results] Compared with the normal group, the mucosal epithelium shedding in the light microscope group showed a large number of inflammatory cell infiltration and ulceration in the mucosa; the microvilli of the epithelial cells in the model group were sparse or even disappeared under the electron microscope; the cell lysis disappeared ; Nuclear pyknosis, cells in the necrotic phase. The protein and mRNA expressions of NLRP-3 and CCL-3 in model group showed an upward trend, which were 1.36 ± 0.25, 1.58 ± 0.17, 1.52 ± 0.16 and 1.49 ± 0.13, respectively, with statistical significance (P <0.05) . [Conclusion] The presence of colorectal mucosa UC induces the high expression of CCL-3 in UC patients. Taking the NLRP-3 inflammasome as the therapeutic target will provide a new idea for the prevention and treatment of UC.