摘要目的 通过构建体内及体外炎症模型,证明前动力蛋白2(PK2)在溃疡性结肠炎中的作用.方法 构建促癌剂甲基偶氮甲烷(AOM)/促炎剂葡聚糖硫酸钠(DSS)诱导的炎症相关性结直肠肿瘤模型,在疾病的不同发展阶段,采用实时定量聚合酶链反应(Real-time PCR)方法检测PK2mRNA表达情况,Western blot法检测其蛋白水平表达,酶联免疫吸附试验(ELISA)法检测结肠组织匀浆中蛋白表达;脂多糖(LPS)诱导NCM460细胞株激活炎症信号通路,分别从mRNA及蛋白水平检测细胞中PK2的表达.结果 在AOM/DSS诱导的炎症相关性结直肠肿瘤模型中,PK2 mRNA及蛋白水平随疾病的进展逐步增加;在LPS诱导的细胞炎症模型中,PK2mRNA及蛋白水平均增加[PK2mRNA升高约3.42倍,P=0.013;PK2蛋白的表达升高约2.10倍,(78.2±5.2) pg/ml比(163.8±8.4)pg/ml;P=0.029].结论 PK2随着炎症的进展表达水平升高,PK2/前动力蛋白受体1(PKR1)信号通路可能在溃疡性结肠炎的发病中发挥重要功能.

abstractsObjective Our object is to determine the significant role of Prokineticin 2 (PK2) in ulcerative colitis through the successful construction of the model of ulcerative colitis in vivo and in vitro.Methods Through the construction of azoxymethane (AOM)/dextran sulfate sodium (DSS) induced colitis-associated colorectal cancer,we detected PK2 mRNA expression by using real-time quantitative polymerase chain reaction (Real-time PCR),the PK2 protein level expression by using Western blotting,and the PK2 protein level expression in colonic homogenate by using enzyme linked immunosorbent assay (ELISA).Induced by lipopolysaccharide (LPS) in NCM460 cell line to activate inflammatory signaling pathway,we detected the expression of PK2 mRNA and protein levels.Results In AOM/DSS induced colitis-associated colorectal cancer model,mRNA and protein levels of PK2 were gradually increased.The mRNA and protein levels of PK2 were increased in LPS induced cellular inflammatory model [PK2 mRNA level elevated approximately 3.42 times,P =0.013;PK2 protein level was increased by about 2.10 times,(78.2±5.2) pg/ml vs.(163.8±8.4) pg/ml,P=0.029].Conclusion With the progression of colitis,PK2 was increased.PK2/prokineticin receptor 1 (PKR1) signaling pathway may play an important function in the pathogenesis of ulcerative colitis.Blocking this pathway may provide a new target for the treatment of ulcerative colitis.