目的 研究蒲黄炭纳米类成分（Typhae Pollen Carbonisatum nano-components，TPC-NCs）对溃疡性结肠炎（ulcerative colitis，UC）的治疗作用及其作用机制。方法 通过透析法从蒲黄炭水煎液中纯化出TPC-NCs，并利用纳米材料表征技术对其形态、光学特性及表面官能团进行表征。采用葡聚糖硫酸钠（dextran sodium sulfate，DSS）诱导建立UC小鼠模型，将30只C57BL/6J小鼠随机分为对照组、模型组、柳氮磺吡啶（sulfasalazine，SASP）组、TPC-NCs组和透析袋外溶液（TPC-O）组。连续给药7 d后，观察小鼠一般情况；评估小鼠疾病活动指数（disease activity index，DAI）；采用苏木素-伊红（hematoxylin-eosin，HE）染色观察结肠组织病理损伤；检测结肠组织髓过氧化物酶（myeloperoxidase，MPO）、超氧化物歧化酶（superoxide dismutase，SOD）活性及肿瘤坏死因子-α（tumor necrosis factor-α，TNF-α）、白细胞介素-1β（interleukin-1β，IL-1β）、IL-6、IL-2、IL-17A、IL-4、IL-10、丙二醛（malondialdehyde，MDA）水平；采用Western blotting检测结肠组织Toll样受体4（Toll-like receptor 4，TLR4）/髓样分化因子88（myeloid differentiation 88，MyD88）/核因子-κB（nuclear factor-κB，NF-κB）信号通路关键蛋白的表达。结果 TPC-NCs粒径集中在1.4～2.2 nm，分散性良好，表面富含羟基、羧基等官能团。体内实验结果显示，TPC-NCs能显著降低UC小鼠的DAI评分（P＜0.01），改善结肠组织病理损伤，降低结肠组织MPO活性及MDA水平（P＜0.01），提高结肠组织中抗氧化酶SOD活性（P＜0.05），抑制促炎因子TNF-α、IL-1β、IL-6、IL-2、IL-17A释放（P＜0.01），上调抗炎因子IL-4、IL-10水平（P＜0.05、0.01），并降低结肠组织TLR4、MyD88、NF-κB p65的蛋白表达水平（P＜0.05、0.01）。结论 TPC-NCs通过抑制TLR4/MyD88/NF-κB信号通路介导的炎症反应，减轻氧化应激损伤，从而发挥对UC的治疗作用。

Objective To investigate the therapeutic effect and mechanism of Typhae Pollen Carbonisatum nano-components (TPC-NCs) on ulcerative colitis (UC). Methods TPC-NCs were purified from the decoction of TPC via dialysis, their morphology, optical properties and surface functional groups were characterized using nanomaterial characterization techniques. A UC mouse model was established using dextran sodium sulfate (DSS), with 30 C57BL/6J mice randomly divided into control group, model group, sulfasalazine (SASP) group, TPC-NCs group, and dialysis bag exterior solution (TPC-O) group. After 7 d of continuous administration, general mouse conditions were observed. Disease activity index (DAI) was evaluated. Hematoxylin-eosin (HE) staining was used to examine colonic histopathological damage. Myeloperoxidase (MPO) and superoxide dismutase (SOD) activities in colonic tissue, as well as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, IL-2, IL-17A, IL-4, IL-10 and malondialdehyde (MDA) levels were measured. Western blotting was employed to assess the expressions of key proteins in Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-κB (NF-κB) signaling pathway in colon tissue. Results TPC-NCs exhibited particle sizes concentrated between 1.4—2.2 nm, with good dispersibility and abundant surface functional groups such as hydroxyl and carboxyl groups. In vivo experimental results demonstrated that TPC-NCs significantly reduced DAI score in UC mice (P < 0.01), improved colonic histopathological damage, decreased MPO activity and MDA level in colon tissue (P < 0.01), enhanced the antioxidant enzyme SOD activity in colonic tissue (P < 0.05), inhibited the release of pro-inflammatory factors TNF-α, IL-1β, IL-6, IL-2 and IL-17A (P < 0.01), up-regulated the levels of anti-inflammatory factors IL-4 and IL-10 (P < 0.05, 0.01), and reduced the protein expression levels of TLR4, MyD88 and NF-κB p65 in colon tissue (P < 0.05, 0.01). Conclusion TPC-NCs exert therapeutic effects on UC by mitigating oxidative stress damage through the suppression of TLR4/MyD88/NF-κB signaling pathway-mediated inflammatory response.

R285.5

泰山产业领军人才项目（Tscx202408173）；中央高校基本科研业务费专项资金资助（2025-XJ-KYQD-002，2024-JYB-JBZD-0400，2024-JYB-JBZD-023，2024-JYB-JBZD-045）