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Amelioration effect of bovine casein glycomacropeptide on ulcerative colitis in mice

机译:牛酪蛋白糖巨肽对小鼠溃疡性结肠炎的改善作用

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To explore the mechanism for amelioration effect of bovine casein glycomacropeptide on oxazolone-induced ulcerative colitis in mice. BALB/c mice were divided into four groups as follows: (1) healthy control, (2) ulcerative colitis model control, (3) casein glycomacropeptide-supplemented ulcerative colitis model (CGMP group), and (4) sulfasalazine-supplemented ulcerative colitis model (SASP group). At the end of the administration period, serum IL-1β, IL-2, IL-4, IL-5, IFN-γ, TNF-α, and IL-10 were measured by cytometric bead array and enzyme-linked immunosorbent assay, and mitogen-activated protein kinase p38 and NF-κB p65 were determined by Western blotting. The results demonstrated the inactivation of NF-κB and MAPK signaling pathways and the downregulation of the serum levels of IL-1β, IL-5, IFN-γ, and TNF-α and upregulation of IL-10 production. These changes may be associated with amelioration of oxazolone-induced ulcerative colitis by bovine casein glycomacropeptide.
机译:探讨牛酪蛋白糖巨肽改善小鼠恶唑酮诱导的溃疡性结肠炎的作用机制。 BALB / c小鼠分为以下四组:(1)健康对照组,(2)溃疡性结肠炎模型对照组,(3)酪蛋白糖巨肽补充性溃疡性结肠炎模型(CGMP组),和(4)柳氮磺吡啶补充的溃疡性结肠炎模型(SASP组)。在给药期结束时,通过细胞计数珠阵列和酶联免疫吸附测定法测定血清IL-1β,IL-2,IL-4,IL-5,IFN-γ,TNF-α和IL-10, Western blot法检测丝裂原活化蛋白激酶p38和NF-κBp65。结果表明,NF-κB和MAPK信号通路失活,血清IL-1β,IL-5,IFN-γ和TNF-α的水平下调以及IL-10产生的上调。这些变化可能与牛酪蛋白糖巨肽改善恶唑酮诱导的溃疡性结肠炎有关。

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