Jiang Chao, Zhu Furong, Aimaier Shabaaiti, Zhang Liang, Ali Md Hasan, Fan Furong, Lu Yating, Jia Mengwei, Wu Dongsen, Yin Haipeng, Wei Jianwang, Chu Shenghui, Liu Min
Key Laboratory of Xinjiang Phytomedicine Resource and Utilisation, Ministry of Education, Institute for Safflower Industry Research, Pharmacy College, Collaborative Innovation Center for Efficient Safflower Production and Resource Utilization of XPCC, Shihezi University, Shihezi 832002, China.
Foods. 2025 Sep 14;14(18):3199. doi: 10.3390/foods14183199.
This study aims to investigate the potential immunological mechanisms by which Safflower polysaccharides (SPSs) regulate colitis. The therapeutic effect of SPSs on colitis was investigated by trinitrobenzene sulfonic acid (TNBS)-induced rats model, TNF-α-stimulated Caco-2 cells, LPS-induced THP-1 cell model, and a co-culture model of Caco-2 and THP-1. The results demonstrated that SPSs effectively ameliorated clinical symptoms, reduced the expression of pro-inflammatory factors, restored colonic pathological damage, regulated the body's immunity, and inhibited intestinal macrophage M1 polarization in vivo. In vitro, SPSs could alleviate the inflammatory response of epithelial cells, inhibit macrophage M1 polarization and regulate epithelial-immune cells interaction. Through the experimental study of siRNA-CHI3L1 and r-CHI3L1, it was found that CHI3L1 mediated the interaction between epithelial cells and immune cells. This study demonstrated that SPS can significantly improve clinical symptoms and alleviated colonic damage in TNBS-induced colitis rat models. The underlying mechanisms are associated with STAT3/NF-κB signaling and immunomodulation, where the immunoregulatory effect is based on CHI3L1-mediated epithelial-immune cell interaction mechanisms.
本研究旨在探讨红花多糖（SPSs）调节结肠炎的潜在免疫机制。通过三硝基苯磺酸（TNBS）诱导的大鼠模型、TNF-α刺激的Caco-2细胞、LPS诱导的THP-1细胞模型以及Caco-2与THP-1的共培养模型，研究SPSs对结肠炎的治疗作用。结果表明，SPSs可有效改善临床症状，降低促炎因子表达，恢复结肠病理损伤，调节机体免疫，并在体内抑制肠道巨噬细胞M1极化。在体外，SPSs可减轻上皮细胞的炎症反应，抑制巨噬细胞M1极化并调节上皮-免疫细胞相互作用。通过对siRNA-CHI3L1和r-CHI3L1的实验研究发现，CHI3L1介导上皮细胞与免疫细胞之间的相互作用。本研究表明，SPS可显著改善TNBS诱导的结肠炎大鼠模型的临床症状并减轻结肠损伤。其潜在机制与STAT3/NF-κB信号传导和免疫调节有关，其中免疫调节作用基于CHI3L1介导的上皮-免疫细胞相互作用机制。
