Objective To investigate the protective effects of Rhizoma polygonati (RP) on dextran sulphate sodium (DSS)-induced ulcerative colitis (UC)and the underlying mechanisms. Methods Thirty-six male C57BL/6 mice were randomly divides into six groups (n=6 per group): control group (CON), model group (DSS), 5-aminosalicylic acid group(5-ASA, 400 mg/(kg·d)), low-dose RP group (RP-L, 2 g/(kg·d)), medium-dose RP group (RP-M, 4 g/(kg·d)], and high-dose RP group (RP-H, 8 g/(kg·d)]. Except for the CON, which received normal drinking water, all other groups were given 3.0 % DSS solution ad libitum for 7 days to induce UC. Starting from day 3 of modeling, the 5-ASA and RP groups were administed with 5-ASA or RP for 7 consecutive days. Body weight was recorded daily, and stool consistency and fecal bleeding were assessed to calculate the disease activity index (DAI) score. At the end of the experiment, mice were euthanized, and colon length was measured. Levels of tumor necrosis factor-α (TNF-α), interleukin (IL) -6, IL-1β, IL-10, and myeloperoxidase (MPO) in colon tissue were determined by enzyme-linked immunosorbent assay (ELISA). Colon tissue injury was evaluated by hematoxylin and eosin (HE) staining. Results Compared with the CON group, RP-H treatment significantly reduced the DAI score (P<0.05), alleviated colon shortening (P<0.05), downregulated the expression of IL-6, IL-1β, and TNF-α, upregulated IL-10 expression (P<0.05), and suppressed MPO activity. Histopathological examination revealed that RP-H intervention attenuated inflammatory cell infiltration and promoted goblet cell regeneration in colon tissue. Conclusion RP can effectively reduce colonic tissue injury in DSS-induced UC mice, party through the suppression of inflammatory responses.
Key words
Rhizoma polygonati /
ulcerative colitis /
inflammatory factors
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References
[1] 周洁, 管咏梅, 李萍, 等. 黄精抗炎活性成分及作用机制研究进展[J]. 中国药学杂志, 2025, 60: 2333–2338.
[2] 管佩瑶, 李子业, 王倩, 等. 黄精多糖的生物学活性及其在相关疾病防治中的作用[J]. 中南大学学报(医学版), 2025, 50: 1664–1673.
[3] 李金玉, 邱宁宁, 易畅, 等. 黄精免疫调节活性及机制的研究进展[J]. 中国实验方剂学杂志, 2025, 31: 298–306.
[4] 张娜娜, 潘慧云, 侯芯芯, 等. 黄精研究现状与可持续发展探析[J]. 安徽农学通报, 2022, 28: 24–26.
[5] 冯宇博, 陈好, 张相安. 中药多糖干预溃疡性结肠炎的作用机制研究进展[J]. 天然产物研究与开发, 2025, 37: 2154–2171.
[6] Li S, Xu X, Pan Y, et al. Integrative multi-omics reveals the anti-colitis mechanisms of polygonatum kingianum collett & hemsl polysaccharides in a mouse DSS model[J]. Nutrients, 2025, 17:2895.
[7] 高兴才,余强.黄精多糖通过调节肠道菌群改善DSS诱导的小鼠结肠炎[C]//中国食品科学技术学会.中国食品科学技术学会第二十一届年会论文摘要集.重庆:2024:260–261
[8] Li H, Wu Y, Zhou Q, et al. Polysaccharide from steamed polygonatum sibiricum ameliorates ulcerative colitis by protecting the intestinal mucosal barrier and regulating gut microbiota[J]. Int J Biol Macromol, 2025, 301: 140343.
[9] 国家中医药管理局、卫生部关于印发医疗机构中药煎药室管理规范的通知(国中医药发〔2009〕3号)[J]. 中华人民共和国卫生部公报, 2009 (6): 29–31.
[10] 简钰乘. 薏苡附子败将散对DSS诱导小鼠溃疡性结肠炎的作用机制研究[D].南昌:江西中医药大学,2023.
[11] 张宏, 王旭昀, 刘美奇, 等. 中药含药血清实验动物灌胃给药剂量探讨[J]. 吉林中医药, 2015, 35: 623–625.
[12] Lv B, Hou L, Zhang H, et al. Pimpinellin mitigates DSS-induced ulcerative colitis in mice by reducing inflammation and regulating gut microbiota[J]. Phytomedicine, 2025, 136: 156308.
[13] Zhao T, Liu S, Ma X, et al. Lycium barbarum arabinogalactan alleviates intestinal mucosal damage in mice by restoring intestinal microbes and mucin O-glycans[J]. Carbohydr Polym, 2024, 330: 121882.
[14] Chen X, Dai P, Zhu Y, et al. A triple-helix white tea polysaccharide alleviates ulcerative colitis via the gut microbiota-metabolites-inflammation regulatory axis[J]. Carbohydr Polym, 2026, 374: 124716.
[15] 孙宇杰, 胡嘉敏, 马敏, 等. 枳连丸水提取物通过调控TLR4/MyD88/NF-κB信号通路减轻溃疡性结肠炎小鼠肠道损伤[J]. 中国病理生理杂志, 2025,41: 331–337.
[16] 孙宇杰, 胡嘉敏, 马敏, 等. 枳连丸水提取物通过调控TLR4/MyD88/NF-κB信号通路减轻溃疡性结肠炎小鼠肠道损伤[J]. 中国病理生理杂志, 2025,41: 331–337.
[17] Liang J, Dai W, Liu C, et al. Gingerenone a attenuates ulcerative colitis via targeting il-17ra to inhibit inflammation and restore intestinal barrier function[J]. Adv Sci (Weinh), 2024, 11: e2400206.
[18] Le Berre C, Roda G,Nedeljkovic Protic M, et al. Modern use of 5-aminosalicylic acid compounds for ulcerative colitis[J]. Expert Opin Biol Ther, 2020, 20: 363–378.
[19] Mehta RS, Mayers JR, Zhang Y, et al. Gut microbial metabolism of 5-ASA diminishes its clinical efficacy in inflammatory bowel disease[J]. Nat Med, 2023, 29: 700–709.
[20] Jang DI, Lee AH, Shin HY, et al. The role of tumor necrosis factor alpha (TNF-α) in autoimmune disease and current TNF-αinhibitors in therapeutics[J]. Int J Mol 2021,22:2719.
[21] Jordan SC, Ammerman N, Choi J, et al. Interleukin-6: an important mediator of allograft injury[J]. Transplantation, 2020, 104: 2497-2506.
[22] Abbas AK, Trotta E, R Simeonov D,,et al. Revisiting IL-2: biology. Revisiting IL-2: biology and therapeutic prospects[J]. Sci Immunol, 2018, 3:eaat1482.
[23] Widodo SS, Dinevska M, Furst LM, et al. IL-10 in glioma[J]. Br J Cancer, 2021, 125: 1466–1476.
[24] Kariyawasam V, Davis T, Ghali M, et al. Myeloperoxidase luminol reaction - a novel faecal assay for predicting colonoscopy findings in patients with ulcerative colitis: a pilot cross-sectional clinical study[J]. Adv Healthc Mater, 2026, 15: e01825.
[25] 唐淼, 袁国栋, 檀金川, 等. 黄精通过调节铁调素来改善2型糖尿病小鼠认知障碍的作用机制研究[J]. 世界中医药, 2025, 20: 1874–1881.
[26] 张敏. 基于传承创新辨证发展观的中药产业现代化研究与实践[D].乌鲁木齐:新疆医科大学,2025.
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