Wu Zhihao, Ma Baohua, Xiao Min, Ren Qian, Shen Yanhua, Zhou Zhengyu
Laboratory Animal Center, Suzhou Medical College, Soochow University, Suzhou 215123, China.
Biology (Basel). 2025 Jun 18;14(6):715. doi: 10.3390/biology14060715.
Although the underlying mechanisms are not yet fully understood, vitamin D has been proven to be associated with the pathogenesis of inflammatory bowel disease, participating in immune response and regulating gut microbiota composition. In this study, we established a dextran sodium sulfate-induced colitis model and intervened with vitamin D. Subsequently, colonic histopathology, serum biochemistry, transcription of inflammatory cytokines, gut microbiota, and key signaling pathways were examined. Our research demonstrated that intervention with vitamin D reduced the disease activity index of DSS-induced colitis and improved histopathological changes, protecting tight junction protein ZO-1 and intestinal glands from damage induced by DSS. Analysis of gut microbiota revealed alterations in both α diversity and β diversity in DSS-induced colitis, whereas interventions with active vitamin D corrected the changes in certain bacterial abundance and improved the composition of gut microbiota. The transcription levels of inflammatory cytokines, including , , -γ, , , and , were elevated in the DSS-induced colitis model. However, intervention with active vitamin D effectively suppressed the transcription of these factors. Finally, immunohistochemistry and Western blotting revealed that the intervention with vitamin D suppressed the expression of proteins associated with the STING pathway, including GATA1, STING, IRF3, and IKBα, leading to inhibition of downstream IFN-β production. Vitamin D administration can ameliorate the severity of DSS-induced colitis by preserving intestinal barrier integrity, modulating gut microbiota composition through suppression of the STING pathway.
尽管其潜在机制尚未完全明确，但维生素D已被证明与炎症性肠病的发病机制相关，参与免疫反应并调节肠道微生物群组成。在本研究中，我们建立了葡聚糖硫酸钠诱导的结肠炎模型并用维生素D进行干预。随后，检测了结肠组织病理学、血清生化指标、炎性细胞因子转录、肠道微生物群及关键信号通路。我们的研究表明，维生素D干预降低了DSS诱导的结肠炎的疾病活动指数，改善了组织病理学变化，保护紧密连接蛋白ZO-1和肠腺免受DSS诱导的损伤。肠道微生物群分析显示，DSS诱导的结肠炎中α多样性和β多样性均发生改变，而活性维生素D干预纠正了某些细菌丰度的变化并改善了肠道微生物群的组成。在DSS诱导的结肠炎模型中，包括 、 、 -γ、 、 、 和 在内的炎性细胞因子的转录水平升高。然而，活性维生素D干预有效抑制了这些因子的转录。最后，免疫组织化学和蛋白质印迹显示，维生素D干预抑制了与STING途径相关的蛋白质的表达，包括GATA1、STING、IRF3和IKBα，导致下游IFN-β产生受到抑制。维生素D给药可通过维持肠道屏障完整性、通过抑制STING途径调节肠道微生物群组成来减轻DSS诱导的结肠炎的严重程度。
