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目的观察补充益生菌对葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎的影响,探讨益生菌对结肠炎的治疗作用和可能机制。方法将小鼠分为4组:正常对照组、DSS组、柳氮磺胺吡啶(SASP)组和双歧杆菌组。建立小鼠急性DSS结肠炎模型。SASP组在饮DSS水同时予SASP灌胃。双歧杆菌组在实验开始前7d予双歧杆菌灌胃至实验结束。每天观察各组疾病活动指数(DAI),并在实验结束后检测各组小鼠炎症肠段肿瘤坏死因子(TNF)α、核因子(NF)κBP65、髓过氧化物酶(MPO)等的表达。结果自实验第4天开始,SASP组和双歧杆菌组DAI明显低于DSS组。实验结束时,SASP组和双歧杆菌组炎症肠段TNFα[(10.01±1.11)和(10.45±0.98)pg·mg-1·ml-1]、MPO[(3.21±0.20)和(3.24±0.16)U/g组织]等的水平较DSS组[(13.35±1.01)pg·mg-1·ml-1和(3.63±0.23)U/g组织]均明显降低,NFκBP65阳性的炎症细胞数减少。结论给小鼠预服双歧杆菌能有效抑制炎症肠段炎症细胞NFκB的活化及炎性细胞因子的分泌,减轻肠道炎症反应。
Objective To observe the effects of probiotics on dextran sodium sulfate (DSS) -induced colitis in mice and explore the therapeutic effect and possible mechanism of probiotics on colitis. Methods The mice were divided into 4 groups: normal control group, DSS group, sulfasalazine (SASP) group and Bifidobacterium group. A mouse model of acute DSS colitis was established. SASP group in the DSS water DSA to SASP gavage. Bifidobacterium group 7d before the start of the experiment to bifidobacteria gavage to the end of the experiment. The disease activity index (DAI) of each group was observed daily, and the expression of tumor necrosis factor (TNF) α, nuclear factor (NF) κBP65, myeloperoxidase (MPO) . Results DAI in SASP group and Bifidobacterium group was significantly lower than that in DSS group from the 4th day of experiment. At the end of the experiment, TNFα [(10.01 ± 1.11) and (10.45 ± 0.98) pg · mg -1 · ml -1], MPO [(3.21 ± 0.20) and (3.24 ± 0.16) ) / U / g tissue] were significantly lower than those in the DSS group [(13.35 ± 1.01) pg · mg-1 · ml-1 and (3.63 ± 0.23) U / g tissues] Conclusion Bifidobacterium pre-treated mice can effectively inhibit the inflammatory bowel inflammatory cells NFκB activation and secretion of inflammatory cytokines, reduce intestinal inflammatory response.