Yam resistant starch protects against ulcerative colitis by modulating short-chain fatty acid-intestinal barrier-immune axis

  • JIA Wenxia ,
  • LI Menglin ,
  • DING Yijie ,
  • QU Xinyan ,
  • LIU Qian ,
  • LI Qingjun ,
  • LIU Hongyan
Expand
  • 1(Shandong University of Traditional Chinese Medicine, 250355, China)
    2(Shandong Analysis and Test Center, Qilu University of Technology (Shandong Academy of Sciences), 250014, China)
    3(Shandong Key Laboratory of Digital Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, 250355, China)
    4(Key Laboratory of Traditional Chinese Medicine Classical Theory, Ministry of Education, Shandong University of Traditional Chinese Medicine, 250355, China)

Received date: 2025-01-26

  Revised date: 2025-04-02

  Online published: 2025-12-15

Abstract

The aim was to prepare yam-resistant starch by a dual enzyme method and to discuss its protective effect on ulcerative colitis.Using yield as an index, an orthogonal experimental design was employed to optimize the yam-resistant starch preparation procedure.A control group, model group, positive drug group, and yam-resistant starch low, medium, and high dosage groups were randomly assigned to sixty C57BL/6 mice.To induce ulcerative colitis in mice, 25 g/L dextran sulfate sodium (DSS) was administered.The mice were noted for their body weights and general health, the colon length was measured, and the disease activity index was computed.The histology of the mouse colon, inflammatory factors, intestinal tight junction protein, mucin expression, transcription factors ROR-γt and Foxp3 mRNA expression, and short-chain fatty acid (SCFA) content were also evaluated.Results indicated that a 20% starch emulsion concentration, 16 U/g pullulanase, 20 U/g heat-resistant α-amylase, and an 18-hour retrogradation interval were the ideal parameters for the manufacture of resistant starch.Of the three treatment groups, the high-dose yam-resistant starch group had the greatest effect.In mice with ulcerative colitis, it significantly decreased colonic histological damage, elevated IL-10 expression, and lowered IL-6, IL-17, and TNF-α expression in comparison to the model group.Furthermore, it enhanced the expression of MUC2 and ZO-1, stimulated the expression of Foxp3 mRNA, suppressed the expression of ROR-γt mRNA, and raised the amount of acetic, propionic, and butyric acids in feces.Therefore, yam resistant starch could improve the amount of short-chain fatty acids in the gut, reduce inflammation, protect the intestinal barrier, restore immunological balance in the gut, and reduce UC symptoms in mice.This could serve as a foundation and guide for the creation of functional foods that prevent and treat ulcerative colitis.

Cite this article

JIA Wenxia , LI Menglin , DING Yijie , QU Xinyan , LIU Qian , LI Qingjun , LIU Hongyan . Yam resistant starch protects against ulcerative colitis by modulating short-chain fatty acid-intestinal barrier-immune axis[J]. Food and Fermentation Industries, 2025 , 51(22) : 163 -171 . DOI: 10.13995/j.cnki.11-1802/ts.042241

References

[1] REUTER M A, TUCKER M, MARFORI Z, et al. Dietary resistant starch supplementation increases gut luminal deoxycholic acid abundance in mice[J]. Gut Microbes, 2024, 16:2315632.
[2] NAN N, WANG D X. Type 2 autoimmune pancreatitis associated with ulcerative colitis[J]. Frontiers in Immunology, 2023, 14:1288390.
[3] 张林瑞, 张文风. 乌梅丸治疗溃疡性结肠炎的研究进展[J/OL]. 中国实验方剂学杂志, 2024. https://link.cnki.net/doi/10.13422/j.cnki.syfjx.20241913.
ZHANG L R, ZHANG W F. Research progress of wumeiwan in treatment of ulcerative colitis[J/OL]. Chinese Journal of Experimental Traditional Medical Formulae, 2024. https://link.cnki.net/doi/10.13422/j.cnki.syfjx.20241913.
[4] LE BERRE C, HONAP S, PEYRIN-BIROULET L. Ulcerative colitis[J]. The Lancet, 2023, 402(10401):571-584.
[5] 丁瑞, 王文秀, 朱远韧, 等. 桃胶多糖对DSS诱导小鼠溃疡性结肠炎的保护作用[J]. 食品工业科技, 2025, 46(14):419-429.
DING R, WANG W X, ZHU Y R, et al. Protective effect of peach gum polysaccharides on DSS-induced ulcerative colitis in mice[J]. Science and Technology of Food Industry, 2025, 46(14):419-429.
[6] ORDÁS I, ECKMANN L, TALAMINI M, et al. Ulcerative colitis[J]. The Lancet, 2012, 380(9853):1606-1619.
[7] KUCHARZIK T, KOLETZKO S, KANNENGIESSER K, et al. Ulcerative colitis-diagnostic and therapeutic algorithms[J]. Deutsches Arzteblatt International, 2020, 117(33-34):564-574.
[8] ZENG W, HE D, XING Y F, et al. Internal connections between dietary intake and gut microbiota homeostasis in disease progression of ulcerative colitis: A review[J]. Food Science and Human Wellness, 2021, 10(2):119-130.
[9] 冯学锋, 黄璐琦, 格小光, 等. 山药道地药材形成源流考[J]. 中国中药杂志, 2008, 33(7):859-862.
FENG X F, HUANG L Q, GE X G, et al. Textual research on origin and development of genuine medicinal herbs of Shanyao[J]. China Journal of Chinese Materia Medica, 2008, 33(7):859-862.
[10] ZHANG X Q, LIANG D, LIU N, et al. Preparation and characterization of resistant starch type 3 from yam and its effect on the gut microbiota[J]. Traditional Medicine Research, 2022, 7(2):11.
[11] NAIK B, KUMAR V, GOYAL S K, et al. Pullulanase: Unleashing the power of enzyme with a promising future in the food industry[J]. Frontiers in Bioengineering and Biotechnology, 2023, 11:1139611.
[12] SUN H J, GUO Y K, WANG H D, et al. Gut commensal Parabacteroides distasonis alleviates inflammatory arthritis[J]. Gut, 2023, 72(9):1664-1677.
[13] HODGKINSON K, EL ABBAR F, DOBRANOWSKI P, et al. Butyrate’s role in human health and the current progress towards its clinical application to treat gastrointestinal disease[J]. Clinical Nutrition, 2023, 42(2):61-75.
[14] ENGLYST H N, KINGMAN S M, CUMMINGS J H. Classification and measurement of nutritionally important starch fractions[J]. European Journal of Clinical Nutrition, 1992, 46(Suppl 2): S33-S50.
[15] SCHIEL-BENGELSDORF B, DÜRRE P. Pathway engineering and synthetic biology using acetogens[J]. FEBS Letters, 2012, 586(15):2191-2198.
[16] MARTIN-GALLAUSIAUX C, MARINELLI L, BLOTTIÈRE H M, et al. SCFA: Mechanisms and functional importance in the gut[J]. Proceedings of the Nutrition Society, 2021, 80(1):37-49.
[17] KOH A, DE VADDER F, KOVATCHEVA-DATCHARY P, et al. From dietary fiber to host physiology: Short-chain fatty acids as key bacterial metabolites[J]. Cell, 2016, 165(6):1332-1345.
[18] LI Y K, LI H Q, WANG R, et al. Protective effect of sodium butyrate on intestinal barrier damage and uric acid reduction in hyperuricemia mice[J]. Biomedicine & Pharmacotherapy, 2023, 161:114568.
[19] ZHAO H R, WANG Q, ZHAO J, et al. Ento-a alleviates DSS-induced experimental colitis in mice by remolding intestinal microbiota to regulate SCFAs metabolism and the Th17 signaling pathway[J]. Biomedicine & Pharmacotherapy, 2024, 170:115985.
[20] LIU Y X, YU Z H, ZHU L P, et al. Orchestration of MUC2-The key regulatory target of gut barrier and homeostasis: A review[J]. International Journal of Biological Macromolecules, 2023, 236:123862.
[21] SUZUKI T. Regulation of the intestinal barrier by nutrients: The role of tight junctions[J]. Animal Science Journal, 2020, 91(1): e13357.
[22] KANG Y, PARK H, CHOE B H, et al. The role and function of mucins and its relationship to inflammatory bowel disease[J]. Frontiers in Medicine, 2022, 9:848344.
[23] 李新科, 杨雪, 张萱, 等. 短链脂肪酸对肠道屏障保护作用的研究进展[J]. 动物营养学报, 2024, 36(8):4861-4871.
LI X K, YANG X, ZHANG X, et al. Research progress on protective effects of short chain fatty acids on intestinal barrier[J]. Chinese Journal of Animal Nutrition, 2024, 36(8):4861-4871.
[24] BILOTTA A J, MA C Y, YANG W J, et al. Propionate enhances cell speed and persistence to promote intestinal epithelial turnover and repair[J]. Cellular and Molecular Gastroenterology and Hepatology, 2021, 11(4):1023-1044.
[25] LIU J Q, XIAO Q, XIAO J N, et al. Wnt/β-catenin signalling: Function, biological mechanisms, and therapeutic opportunities[J]. Signal Transduction and Targeted Therapy, 2022, 7:3.
[26] XU M, POKROVSKII M, DING Y, et al. C-MAF-dependent regulatory T cells mediate immunological tolerance to a gut pathobiont[J]. Nature, 2018, 554(7692):373-377.
[27] BYNDLOSS M X, OLSAN E E, RIVERA-CHÁVEZ F, et al. Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion[J]. Science, 2017, 357(6351):570-575.
Outlines

/