维生素D通过使用JAKSTAT信号通路调节肠道微生物群和免疫微环境来抑制结直肠癌癌症细胞的发育
Vitamin D inhibits the development of colorectal cancer cells by regulating the gut microbiota and immune microenvironment using JAKSTAT signaling pathway.
摘要(中文译文)
探讨维生素D是否通过维生素D受体（VDR）-JAK-STAT信号通路调控肠道菌群及结直肠癌（CRC）免疫微环境。将30只雄性SD大鼠随机分为对照组（CG）、模型组（MG）和维生素D干预组（VDG）。比较各组VDR-JAK-STAT通路蛋白表达水平（VDR、p-JAK2/JAK2、p-STAT3/STAT3）、肠道菌群组成（16S rRNA测序）及免疫标志物（CD4/CD8 T细胞、调节性T细胞（Treg）、白细胞介素（IL）-6、IL-10、肿瘤坏死因子（TNF）-α）。与CG相比，MG的VDR表达显著降低（<0.05），p-JAK2/JAK2和p-STAT3/STAT3比值显著升高（<0.05）。肠道菌群α多样性（Shannon/Chao1指数）显著降低（<0.05），菌群组成异常，表现为……减少及……/……增加（<0.05）。免疫微环境失衡表现为CD4 T细胞减少（<0.05）、Treg细胞增加（<0.05）、促炎细胞因子IL-6/TNF-α升高及抗炎细胞因子IL-10降低（<0.05）。维生素D干预显著逆转了上述异常（均<0.05）。MG还表现为巨噬细胞比例及M2极化显著增加，树突状细胞比例及M1巨噬细胞极化显著降低（均<0.01）。维生素D干预逆转了极化失衡，减少总巨噬细胞、增加M1极化并减少M2极化（均<0.05）。维生素D通过激活VDR抑制JAK-STAT通路的过度激活，改善肠道菌群失调，恢复丁酸盐代谢，并重新平衡巨噬细胞极化。
Abstract
To investigate whether vitamin D modulates gut microbiota and the colorectal cancer (CRC) immune microenvironment through the vitamin D receptor (VDR)-JAK-STAT signaling pathway. Thirty male SD rats were randomly divided into the control group (CG), model group (MG), and vitamin D intervention group (VDG). Protein expression levels of VDR-JAK-STAT pathway (VDR, p-JAK2/JAK2, p-STAT3/STAT3), gut microbiota composition ( 16S rRNA sequencing), and immune markers (CD4/CD8 T cells, regulatory T cells (Treg), interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-α were compared across the groups. Compared to the CG, the MG exhibited a significant reduction in VDR expression ( < 0.05) and a marked increase in the p-JAK2/JAK2 and p-STAT3/STAT3 ratios ( < 0.05). The gut microbiota α-diversity (Shannon/Chao1 indices) was significantly reduced ( < 0.05), and microbial composition was abnormal, with a decrease in and an increase in / ( < 0.05). Immune microenvironment imbalance was characterized by a reduction in CD4 T cells ( < 0.05), an increase in Treg cells ( < 0.05), elevated pro-inflammatory cytokines IL-6/TNF-α, and decreased anti-inflammatory cytokine IL-10 ( < 0.05). Vitamin D intervention significantly reversed these abnormalities (all < 0.05). The MG also showed a significant increase in macrophage proportion and M2 polarization, and a significant decrease in dendritic cell proportion and M1 macrophage polarization (all < 0.01). Vitamin D intervention reversed the polarization imbalance, reducing total macrophages, increasing M1 polarization, and decreasing M2 polarization (all < 0.05). Vitamin D inhibits excessive activation of the JAK-STAT pathway through VDR activation, ameliorates gut microbiota dysbiosis, restores butyrate metabolism, and rebalances macrophage polarization.
如何引用
AMA
Geyan Bai, Yinglong Tao, Min Fan. Vitamin D inhibits the development of colorectal cancer cells by regulating the gut microbiota and immune microenvironment using JAKSTAT signaling pathway.. Immunopharmacology and immunotoxicology. 2026; doi:10.1080/08923973.2026.2630162.
APA
Geyan Bai, Yinglong Tao, Min Fan (2026). Vitamin D inhibits the development of colorectal cancer cells by regulating the gut microbiota and immune microenvironment using JAKSTAT signaling pathway.. Immunopharmacology and immunotoxicology. https://doi.org/10.1080/08923973.2026.2630162
GB/T 7714
Geyan Bai, Yinglong Tao, Min Fan. Vitamin D inhibits the development of colorectal cancer cells by regulating the gut microbiota and immune microenvironment using JAKSTAT signaling pathway.[J]. Immunopharmacology and immunotoxicology, 2026 doi:10.1080/08923973.2026.2630162.
在 PubMed增强版 阅读全文
翻译全文 · AI 文献问答 · PDF 原文下载 · 引用导出