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口服半乳糖寡糖制剂可抑制 NC/Nga 小鼠特应性皮炎样皮肤损伤的发展。

Oral administration of a galactooligosaccharide preparation inhibits development of atopic dermatitis-like skin lesions in NC/Nga mice.

机构信息

Graduate School of Biosphere Science, Hiroshima University, Higashi-Hiroshima 739-8528, Japan.

出版信息

Int J Mol Med. 2010 Mar;25(3):331-6. doi: 10.3892/ijmm_00000349.

DOI:10.3892/ijmm_00000349
PMID:20127036
Abstract

Anti-allergic effects of galactooligosaccharide (GOS), which is found in breast milk and frequently added to food for promoting health, were evaluated in a human-like mouse model of atopic dermatitis (AD). NC/Nga mice were fed 5.5% GOS for 8 weeks, and we examined whether this treatment suppressed the development of AD-like skin lesions in these mice. Mice fed GOS exhibited significantly less symptoms of dermatitis, reduced scratching frequency, and lower levels of serum total immunoglobulin E compared to control. At the end of the 8-week-experimental period, spleens were removed, and the splenocytes were stimulated with phorbol 12-myristate 13-acetate and ionomycin, following which production of cytokines and a chemokine was analyzed. Elevated levels of Th1 cytokines such as interferon-gamma were observed in splenocytes from GOS-fed mice. However, the levels of Th2 cytokines such as interleukin (IL)-13 were unchanged. Furthermore, GOS inhibited the production of inflammatory cytokines such as IL-1beta, IL-6, IL-17, and tumor necrosis factor-alpha but enhanced production of immunomodulatory IL-10. The results indicate that GOS effectively blocked AD-like skin lesions in the mice by at least partly inducing production of IL-10 and suppressing the production of cytokines such as IL-17, which are involved in skin inflammation.

摘要

半乳糖寡糖(GOS)存在于母乳中,常被添加到食品中以促进健康,其抗过敏性在特应性皮炎(AD)的人类样小鼠模型中得到了评估。NC/Nga 小鼠用 5.5% GOS 喂养 8 周,我们检测了这种治疗是否抑制了这些小鼠 AD 样皮肤损伤的发展。与对照组相比,用 GOS 喂养的小鼠表现出明显较少的皮炎症状、减少的搔抓频率和较低的血清总免疫球蛋白 E 水平。在 8 周实验期结束时,取出脾脏,用佛波醇 12-肉豆蔻酸 13-乙酸酯和离子霉素刺激脾细胞,然后分析细胞因子和趋化因子的产生。从 GOS 喂养的小鼠的脾细胞中观察到 Th1 细胞因子(如干扰素-γ)的水平升高。然而,Th2 细胞因子(如白细胞介素(IL)-13)的水平没有变化。此外,GOS 抑制了促炎细胞因子(如白细胞介素(IL)-1β、IL-6、IL-17 和肿瘤坏死因子-α)的产生,但增强了免疫调节细胞因子 IL-10 的产生。结果表明,GOS 通过至少部分诱导 IL-10 的产生并抑制参与皮肤炎症的细胞因子(如 IL-17)的产生,有效地阻止了小鼠的 AD 样皮肤损伤。

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