Bmi-1通过下调NF-κB信号通路防治小鼠萎缩性胃炎

Bmi-1 protects mice from atrophic gastritis by down-regulating NF-κB signaling pathway

目的:明确Bmi-1是否有防治萎缩性胃炎的作用及其机制。方法:针对7周龄Bmi-1基因缺失(Bmi-1 knock out,BKO)纯合子小鼠和同窝野生型(wild type,WT)小鼠,利用组织学切片、免疫组织化学和Western blot比较分析胃的表型差异。结果:与WT小鼠相比,BKO小鼠表现为胃壁变薄、腺体萎缩和炎症浸润的萎缩性胃炎表型。免疫组化结果显示白细胞介素6(interleukin 6,IL-6)、肿瘤坏死因子α(tumor necrosis factorα,TNF-α)阳性细胞面积和核因子-κB-p65(nuclear factor-κB-p65,NF-κB-p65)阳性细胞数明显增加;Western blot结果显示IL-6、TNF-α和NF-κB-p65蛋白表达水平明显升高。结论:在小鼠中,Bmi-1可通过下调NF-κB信号通路防治萎缩性胃炎。

Objective： To investigate the role of Bmi- 1 in preventing atrophic gastritis in mice. Methods： The phenotype of stomach was compared between wild-type and Bmi- 1 gene knock-out mice at 7 weeks of ages by histology, immunohistochemistry and Westernblot. Resuhs： Bmi-1 gene knock-out mice displayed thin gastric wall, inflammatory infiltration in gastric mucosa and atrophy of gastric gland. The expression of interleukin-6（IL-6） ,tumor necrosis factor α（TNF-α） and nuclear factor-κB-p65 （NF-κB-p65） is up-regulated in Bmi-1 knock-out mice. Conclusion：Bmi-1 could protect mice from atrophic gastritis by down-regulating NF-κB signaling pathway.