Zhang Yuxin, Deng Zeyuan, Li Hongyan, Jiang Zeyin
State Key Laboratory of Food Science and Resources, Nanchang University, Nanchang 330047, China.
International Institute of Food Innovation, Nanchang University, Nanchang 330051, China.
Foods. 2025 Mar 23;14(7):1110. doi: 10.3390/foods14071110.
Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by recurrent episodes and an inability to achieve a complete cure. The spermidine derivative (di--coumaroyl-caffeoyl spermidine, SPDD), as a key alkaloid, exhibits unique health benefits. However, it has not yet been reported whether SPDD can improve dextran sulfate sodium (DSS)-induced colitis in mice. Herein, we investigated the effects and mechanisms of SPDD on DSS-induced colitis in mice. SPDD was successfully purified from rose bee pollen and was found to have a protective effect on colitis, evidenced by reduced disease activity index (DAI) scores and colonic inflammation, increased colonic length and upregulated the expression of tight junction proteins (TJs) in the model ( < 0.05). Importantly, the IL-17 signaling pathway showed significant enrichment by RNA sequencing (RNA-seq) technology with SPDD treatment, which resulted in the downregulation of MAPK4 expression ( < 0.05). Furthermore, SPDD weakened the interaction between MAPK4 and AKT, resulting in a decrease in the phosphorylation level of AKT, thereby reducing the expression of IL-6, IL-1β, iNOS, and COX-2, and alleviating colitis ( < 0.05). In addition, SPDD treatment also ameliorated TNF-α-induced inflammation in Caco-2 cells. Overall, our study demonstrated that SPDD reversed colonic inflammation in colitis mice through the MAPK4/AKT pathway and might be a promising candidate for UC intervention.
溃疡性结肠炎（UC）是一种慢性炎症性肠病，其特征为反复发作且无法完全治愈。亚精胺衍生物（二 - 香豆酰 - 咖啡酰亚精胺，SPDD）作为一种关键生物碱，具有独特的健康益处。然而，尚未有关于SPDD是否能改善葡聚糖硫酸钠（DSS）诱导的小鼠结肠炎的报道。在此，我们研究了SPDD对DSS诱导的小鼠结肠炎的影响及其机制。SPDD成功从玫瑰蜂花粉中纯化出来，并且发现其对结肠炎具有保护作用，表现为疾病活动指数（DAI）评分降低、结肠炎症减轻、结肠长度增加以及模型中紧密连接蛋白（TJ）的表达上调（<0.05）。重要的是，通过RNA测序（RNA-seq）技术发现，SPDD处理使IL-17信号通路显著富集，这导致MAPK4表达下调（<0.05）。此外，SPDD减弱了MAPK4与AKT之间的相互作用，导致AKT磷酸化水平降低，从而减少IL-6、IL-1β、诱导型一氧化氮合酶（iNOS）和环氧化酶-2（COX-2）的表达，并减轻结肠炎（<0.05）。此外，SPDD处理还改善了肿瘤坏死因子-α（TNF-α）诱导的Caco-2细胞炎症。总体而言，我们的研究表明，SPDD通过MAPK4/AKT途径逆转了结肠炎小鼠的结肠炎症，可能是UC干预的一个有前景的候选药物。
