食品科学 ›› 2026, Vol. 47 ›› Issue (11): 140-150.doi: 10.7506/spkx1002-6630-20251223-188

• 营养卫生 • 上一篇    

唾液酸与3’-唾液酸乳糖对葡聚糖硫酸钠诱导小鼠结肠炎的改善作用

巢诚,周启文,纳凯,张莉,郭小华   

  1. (中南民族大学生命科学学院,湖北 武汉 430074)
  • 发布日期:2026-07-02
  • 基金资助:
    湖北省新工科实践基地建设项目(XGK04019);湖北省工程硕博士校企联合培养实践项目(HZY25113); 中南民族大学学术创新团队项目(XTZ24023)

Ameliorative Effects of Sialic Acid and 3’-Sialyllactose against Dextran Sulfate Sodium-Induced Colitis in Mice

CHAO Cheng, ZHOU Qiwen, NA Kai, ZHANG Li, GUO Xiaohua   

  1. (College of Life Sciences, South-Central Minzu University, Wuhan 430074, China)
  • Published:2026-07-02

摘要: 目的:探讨唾液酸(sialic acid,SA)与3’-唾液酸乳糖(3’-sialyllactose,3’-SL)对葡聚糖硫酸钠(dextran sulfate sodium,DSS)诱导小鼠结肠炎的缓解作用及肠道微生物结构的影响。方法:本研究选用48 只4~5 周龄SPF级C57BL/6雄性小鼠,随机分为4 组(每组12 只):CON组每日灌胃磷酸盐缓冲液;DSS组前21 d饮用磷酸盐缓冲液,第22~29天饮用0.025 g/mL DSS水溶液;DSS+SA、DSS+3’-SL组前21 d饮水中分别添加2 mg/mL SA、2 mg/mL 3’-SL,第22~29天均饮用0.025 g/mL DSS水溶液。自第22天起记录小鼠体质量、粪便性状及出血情况;第29天麻醉处死,取血清、结肠组织及内容物进行后续检测分析。结果:SA与3’-SL干预可回升小鼠体质量、增加结肠长度、减轻水肿,显著降低疾病活动指数(P<0.05),同时上调紧密连接蛋白与黏蛋白表达,降低结肠及血清炎症因子水平。门水平上,与DSS组相比,SA与3’-SL均可上调Firmicutes、下调Verrucomicrobiota丰度且组间差异显著(P<0.05)。种水平上,DSS+SA组主要富集Akkermansia muciniphila、Muribaculum intestinale、Turicibacter sanguinis,DSS+3’-SL组主要富集A. muciniphila、Monoglobus pectinilyticus、Lactobacillus murinus。结论:SA与3’-SL均能缓解DSS诱导的结肠炎,二者作用机制存在差异:SA直接作用于宿主屏障与免疫调节,3’-SL通过寡糖结构特异性富集有益菌、重构菌群平衡,其益生功能并非完全依赖代谢产物SA,二者具有机制互补性,为其作为功能性食品原料的精准营养配伍提供理论依据。

关键词: 唾液酸;3’-唾液酸乳糖;葡聚糖硫酸钠;肠道损伤;肠道微生物

Abstract: Purpose: This study aimed to investigate the alleviating effects of sialic acid (SA) and 3’-sialyllactose (3’-SL) on dextran sulfate sodium (DSS)-induced colitis in mice and to evaluate their influence on the intestinal microbiota structure. Methods: Forty-eight specific pathogen-free (SPF) male C57BL/6 mice (4–5 weeks old) were randomly divided into 4 groups (n = 12/group): a control (CON) group, which received daily intragastric administration of phosphate-buffered saline; a DSS group, which drank water from day 1 to 21 and then drank 0.025 g/mL DSS aqueous solution from day 22 to 29; and a DSS + SA and a DSS + 3’-SL group, which drank water containing 2 mg/mL SA and 2 mg/mL 3’-SL from day 1 to 21 and then 0.025 g/mL DSS aqueous solution, respectively. Body mass, fecal traits and bleeding status of mice were recorded daily from day 22 onwards. On day 29, the mice were anesthetized and sacrificed. Serum, colon tissues and colonic contents were collected for subsequent detection and analysis. Results: Intervention with SA and 3’-SL restored mouse body mass, increased colon length, alleviated edema, and significantly reduced disease activity index (DAI) (P < 0.05). Both SA and 3’-SL upregulated the expression of tight junction proteins and mucins, and decreased the levels of inflammatory factors in the colon and serum. At the phylum level, compared with the DSS group, both SA and 3’-SL upregulated the abundance of Firmicutes and downregulated the abundance of Verrucomicrobiota, with significant differences between groups (P < 0.05). At the species level, the DSS + SA group was enriched with Akkermansia muciniphila, Muribaculum intestinale and Turicibacter sanguinis, while the DSS + 3’-SL group was enriched with A. muciniphila, Monoglobus pectinilyticus, and Lactobacillus murinus. Both SA and 3’-SL alleviated DSS-induced colitis in mice, but there were differences in their mechanisms of action. SA acted directly on the host intestinal barrier and immune regulation, while 3’-SL specifically enriched beneficial bacteria and reshaped intestinal microbial balance through its oligosaccharide structure. Conclusion: The probiotic function of 3’-SL is not entirely dependent on its metabolic product SA, and the two compounds have complementary mechanisms of action. This provides a theoretical basis for the precise nutritional combination of SA and 3’-SL as functional food ingredients.

Key words: sialic acid; 3’-sialyllactose; dextran sulfate sodium; intestinal injury; gut microbiota

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