Zhang Xiuli, Zhang Hao, Wang Jingting, Chen Yangyi, Lin Jiumao, Wang Qingshui, Wu Cheng, Chen Hui, Lin Yao
College of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China.
Basic Medical Experimental Teaching Center, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian, China.
Biofactors. 2025 Jan-Feb;51(1):e70001. doi: 10.1002/biof.70001.
Curcumin, a compound from Curcuma longa L., has significant anti-inflammatory properties. However, the mechanisms underlying its anti-inflammatory activity in dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) remain inadequately understood. This study aimed to further elucidate the molecular mechanisms of curcumin DSS-induced UC mice. Our data showed that curcumin alleviated DSS-induced colitis by reducing intestinal damage and inflammation, increasing goblet cells in colon tissues. Enzyme-linked immunosorbent assay revealed that curcumin reduced the expression of inflammatory cytokines (tumor necrosis factor-alpha, interleukin-1β, and interleukin-8) in serum and myeloperoxidase in colon tissues. A comprehensive analysis integrating network pharmacology and RNA sequencing (RNA-seq) revealed significant enrichment of the nuclear factor kappa B (NF-κB) signaling pathways. Notably, RNA-seq analysis demonstrated that curcumin significantly downregulated the mRNA expression of sphingosine kinase 1 (SphK1). Furthermore, molecular docking analysis showed that curcumin can bind to SphK1 and NF-κB. Additionally, curcumin was found to inhibit the activation of the SphK1/NF-κB signaling pathway in DSS-induced UC colon tissue. This study addresses pharmacologic and mechanistic perspectives of curcumin that ameliorates DSS-induced UC and inflammatory response.
姜黄素是一种从姜黄中提取的化合物，具有显著的抗炎特性。然而，其在葡聚糖硫酸钠（DSS）诱导的溃疡性结肠炎（UC）中的抗炎活性机制仍未得到充分理解。本研究旨在进一步阐明姜黄素对DSS诱导的UC小鼠的分子机制。我们的数据表明，姜黄素通过减少肠道损伤和炎症、增加结肠组织中的杯状细胞来减轻DSS诱导的结肠炎。酶联免疫吸附测定显示，姜黄素降低了血清中炎症细胞因子（肿瘤坏死因子-α、白细胞介素-1β和白细胞介素-8）的表达以及结肠组织中髓过氧化物酶的表达。综合网络药理学和RNA测序（RNA-seq）的全面分析显示核因子κB（NF-κB）信号通路显著富集。值得注意的是，RNA-seq分析表明姜黄素显著下调了鞘氨醇激酶1（SphK1）的mRNA表达。此外，分子对接分析表明姜黄素可以与SphK1和NF-κB结合。此外，发现姜黄素可抑制DSS诱导的UC结肠组织中SphK1/NF-κB信号通路的激活。本研究探讨了姜黄素改善DSS诱导的UC和炎症反应的药理学和机制方面。
