食品科学 ›› 2025, Vol. 46 ›› Issue (18): 155-147.doi: 10.7506/spkx1002-6630-20250222-107

• 营养卫生 • 上一篇    下一篇

低聚甘露糖改善特应性皮炎及其诱发的心理合并症

聂婷婷,陈悦,汤柳,陈少泽,方明玉,方振峰,施璐,曹晓琴   

  1. (1.江汉大学医学部药学院,认知与情感障碍湖北省重点实验室,江汉大学医学部湖北省医学实验教学示范中心,湖北?武汉 430100;2.武汉大学人民医院药剂科,湖北?武汉 430100)
  • 出版日期:2025-09-25 发布日期:2025-08-19
  • 基金资助:
    江汉大学2023年省级大学生创新训练项目(S202311072095)

Mannan Oligosaccharides Improve Atopic Dermatitis and Its Psychological Comorbidities

NIE Tingting, CHEN Yue, TANG Liu, CHEN Shaoze, FANG Mingyu, FANG Zhenfeng, SHI Lu, CAO Xiaoqin   

  1. (1. Hubei Key Laboratory of Cognitive and Affective Disorders, Hubei Provincial Demonstration Center for Experimental Medicine Education, College of Pharmacy, School of Medicine, Jianghan University, Wuhan 430100, China; 2. Department of Pharmacy, Renmin Hospital of Wuhan University, Wuhan 430100, China)
  • Online:2025-09-25 Published:2025-08-19

摘要: 目的:探讨特应性皮炎(atopic dermatitis,AD)与肠道菌群、AD诱发焦虑抑郁行为之间的关联,并评估低聚甘露糖(mannan oligosaccharides,MOS)通过调节菌群和短链脂肪酸治疗AD的潜力。方法:用2,4-二硝基氟苯诱导雌性昆明小鼠AD症状,每天口服MOS,共14 d。造模第6天和第11天记录小鼠瘙痒次数,在小鼠解剖后测量表皮厚度、肥大细胞浸润情况及血清中炎症因子水平。此外对脑部5-羟色胺(5-hydroxytryptamine,5-HT)和去甲肾上腺素(norepinephrine,NE)等神经递质水平进行检测,并对粪便中的肠道菌群丰度和短链脂肪酸(short-chain fatty acids,SCFAs)含量进行分析。结果:MOS可以通过降低炎症因子水平显著减轻AD症状,这反映在AD小鼠抓挠次数、表皮厚度、肥大细胞和炎症因子含量的显著下降。MOS干预能够上调5-HT和NE等神经递质表达,从而改善AD小鼠焦虑和抑郁行为。此外,与AD组相比,MOS干预可以增加小鼠肠道微生物群的丰度,特别是双歧杆菌、乳酸杆菌和克雷伯氏菌等有益菌。同时,这些有益菌显著提高了AD小鼠粪便中SCFAs的含量,尤其是丙酸的含量。相关性分析表明,AD的改善与SCFAs水平和某些肠道微生物的增殖呈正相关。结论:MOS干预可能为治疗AD及其诱发的心理合并症提供一种新的方法。

关键词: 低聚甘露糖;特应性皮炎;焦虑和抑郁行为;肠道微生物群

Abstract: Objective: This study aimed to investigate the association of atopic dermatitis (AD) and anxiety/depression behaviors induced by AD with the intestinal microbiota. Additionally, it sought to evaluate the therapeutic potential of mannan oligosaccharide (MOS) in alleviating AD symptoms through the modulation of the gut microbiota and the enhancement of short-chain fatty acids (SCFAs) production. Methods: Female Kunming mice were challenged with 2,4-dinitrofluorobenzene (DNFB) to induce AD-like symptoms. MOS was administered orally daily for 14 days. On the 6th and 11th days post-modeling, the number of scratching bouts in mice was recorded. Following dissection, epidermal thickness, mast cell infiltration, and serum levels of inflammatory cytokines were measured. Meanwhile, cerebral levels of neurotransmitters, including 5-hydroxytryptamine (5-HT) and norepinephrine (NE), were assessed. The abundance of intestinal microbiota and fecal concentrations of SCFAs were also analyzed. Results: MOS significantly reduced AD-like symptoms by reducing inflammatory cytokines, as reflected in a significant decrease in the number of scratching bouts, epidermal thickness, mast cells and inflammatory cytokine levels. MOS intervention up-regulated the expression of 5-HT and NE, and consequently alleviated anxiety and depression-like behaviors. Furthermore, compared with the AD group, MOS intervention increased the gut microbiota abundance of mice, especially beneficial bacteria such as Bifidobacterium, Lactobacillus and Klebsiella. At the same time, these beneficial bacteria significantly increased the fecal contents of SCFAs, especially propionic acid. Correlation analysis indicated that AD amelioration was positively correlated with fecal SCFAs levels and the proliferation of certain intestinal microbes. Conclusion: MOS intervention could offer a novel approach to managing AD and its psychological comorbidities.

Key words: mannan oligosaccharides; atopic dermatitis; anxiety and depression-like behaviors; gut microbiota

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