Bmi⁃1 protects mice from atrophic gastritis by down⁃regulating NF⁃κB signaling pathway
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摘要:
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 factor α，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。
Abstract:
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 Western-blot. Results：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.
