- 期刊Journal of agricultural and food chemistry（J Agric Food Chem）
- 发表时间2026-09-23
- 作者Tian W, Chu W, Liu Y, Zhou Z, Zhong R, Cao Y, Xiao J
- 卷期页码V74(37) : 29211-29223
- DOI10.1021/acs.jafc.6c04431
- PMID42916518
摘要机译
溃疡性结肠炎（UC）需要同时恢复上皮屏障完整性和抑制粘膜炎症的治疗策略。在这里，我们开发了一种结肠靶向微粒MC（6G+PIP），以同步递送6-姜酚（6G）和胡椒碱（PIP）。纳米结构脂质载体被壳聚糖和魔芋葡甘聚糖包被，形成微球（10.5μm），封装效率超过90%。
MC（6G+PIP）可防止胃和肠液中的过早释放（<15%），同时可持续结肠释放6G（82.91%）和PIP（81.64%）。与MC（6G）相比，在DSS诱导的结肠炎小鼠中，MC（6G+PIP）可加速体重恢复（1.9倍），降低疾病活动（2.62倍），并降低肠道通透性50%。
机制上，共递送与色氨酸衍生的吲哚代谢物增加（分别为1.66倍和3.28倍vs MC（6G）和MC（PIP））和AhR-Cyp1a1轴的激活有关，有助于改善上皮修复和减少炎症。这些发现突出了一种将靶向递送与微生物群调节相结合的新方法，可用于有效的UC治疗。
展开英文摘要原文
Ulcerative colitis (UC) requires therapeutic strategies that concurrently restore epithelial barrier integrity and suppress mucosal inflammation. Here, we developed a colon-targeted microparticle MC(6G+PIP) to synchronize the delivery of 6-gingerol (6G) and piperine (PIP). Nanostructured lipid carriers were coated with chitosan and konjac glucomannan to form microspheres (∼10.5 μm) with encapsulation efficiencies exceeding 90%. MC(6G+PIP) prevented premature release in gastric and intestinal fluids (<15%), while enabling sustained colonic release of 6G (82.91%) and PIP (81.64%). In DSS-induced colitis mice, MC(6G+PIP) accelerated body weight recovery (1.9-fold), reduced disease activity (2.62-fold), and lowered intestinal permeability by ∼50% as compared to MC(6G). Mechanistically, codelivery was associated with increased tryptophan-derived indole metabolites (1.66- and 3.28-fold vs MC(6G) and MC(PIP), respectively) and activation of the AhR-Cyp1a1 axis, contributing to improved epithelial repair and reduced inflammation. These findings highlighted a novel approach that combines targeted delivery with microbiota modulation for effective UC therapy.
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