Probiotics are known to be beneficial in preventing different diseases in model animals, including inflammatory bowel disease. However, there are few studies on probiotics related to miRNA regulation and disease status. In this article, the beneficial role and mechanisms of the probiotic strain Bifidobacterium bifidum ATCC 29521 have been studied in ulcerative colitis using dextran sodium sulphate (DSS) model. Male C57JBL/6 mice were randomly divided into three groups (n=7): Normal group, dextran sulphate sodium (DSS) group, and Bifido group gavage with Bifidobacterium bifidum ATCC 29521 (2×10⁸ CFU/day). Our strain restored the DSS-caused damage by regulating the expression of immune markers and tight junction proteins (TJP) in the colon; briefly by up-regulating ROS-scavenging enzymes (SOD1, SOD2, CAT, and GPX2), anti-inflammatory cytokines (IL-10, PPARγ, IL-6), TJP's (ZO-1, MUC-2, Claudin-3, and E Cadherin-1) and downregulating inflammatory genes (TNF-α, IL-1β) in Bifido group mice. Inflammatory markers appeared to be regulated by NF-κB nuclear P65 subunit, and its translocation was inhibited in Bifido group mice colon. In addition, the expression of inflammatory genes and colonic TJP were also associated with the restoration of miRNAs (miR-150, miR-155, miR-223) in B. bifidum ATCC 29521 treated Bifido group. The dysbiosis executed by DSS was restored in the Bifido group, demonstrating that B. bifidum ATCC 29521 possessed a probiotic role in our DSS colitis mouse model. B. bifidum ATCC 29521 exhibited its probiotic role through its anti-inflammatory role by modulating miRNA-associated TJP and NF-κB regulation and by partially restoring dysbiosis.

已知益生菌有益于预防模型动物的各种疾病，包括炎症性肠病。但是，关于与miRNA调节和疾病状态有关的益生菌的研究很少。在本文中，已使用右旋糖酐硫酸钠（DSS）模型研究了益生菌双歧双歧杆菌ATCC 29521在溃疡性结肠炎中的有益作用和机制。将雄性C57JBL / 6小鼠随机分为三组（n = 7）：正常组，葡聚糖硫酸钠（DSS）组和用双歧双歧杆菌ATCC 29521灌胃的Bifido组（2×10 ⁸CFU /天）。我们的菌株通过调节结肠中免疫标志物和紧密连接蛋白（TJP）的表达来恢复DSS造成的损伤。通过上调ROS清除酶（SOD1，SOD2，CAT和GPX2），消炎细胞因子（IL-10，PPARγ，IL-6），TJP（ZO-1，MUC-2，Claudin-3，和E Cadherin-1）和下调炎症基因（TNF-α，IL-1β）在Bifido组小鼠中。炎性标志物似乎受NF-κB核P65亚基的调节，在Bifido组小鼠结肠中其易位受到抑制。另外，在双歧双歧杆菌ATCC 29521治疗的Bifido组中，炎症基因和结肠TJP的表达也与miRNA（miR-150，miR-155，miR-223）的恢复有关。在双歧杆菌组中，由DSS执行的营养不良得以恢复，表明双歧双歧杆菌ATCC 29521在我们的DSS结肠炎小鼠模型中具有益生菌作用。双歧双歧杆菌ATCC 29521通过调节miRNA相关的TJP和NF-κB的调节以及部分恢复营养不良而具有抗炎作用，从而表现出其益生菌作用。