已知肠道微生物组和胆汁酸代谢的改变在结肠癌的发生和进展中发挥作用。药用植物如黄芪和姜黄。 (AC)对癌症治疗，特别是结肠癌等消化道肿瘤显示出较好的治疗效果。然而，AC 抑制结肠癌的确切机制，特别是与肠道微生物组和胆汁酸动态相关的确切机制尚未完全了解。我们的研究旨在研究 AC 对 CT26 结肠癌小鼠的抗肿瘤特性，并进一步研究其作用。通过肠道微生物群的潜在机制。通过结肠癌实体瘤的大小和病理变化来评价AC对结肠癌的抑制作用。采用宏基因组学和16s rRNA基因测序来阐明结肠癌肠道微生物群的失调及其对结肠癌的影响。采用UPLC-Qtrap-MS/MS检测各组小鼠粪便中胆汁酸（BA）的水平。AC有效抑制结肠癌的生长，减少组织学损伤。值得注意的是，AC 治疗导致肠道微生物组组成发生变化，柠檬酸杆菌和 Candidatus_Arthromitus 等致病菌减少，而 Adlercreutzia、Lachnospiraceae_UCG-001 和 Parvibacter 等有益微生物种群增加。此外，AC 改变了胆汁酸分布，导致促癌胆汁酸（例如脱氧胆酸 (DCA) 和石胆酸 (LCA)）显着减少，同时增加了抗癌胆汁酸熊去氧胆酸 (UDCA) 的浓度。跟踪分析数据发现，AC可能主要通过增加Adlercreutzia和Parvibacter细菌的相对丰度来上调FabG和baiA基因，从而促进促癌LCA的代谢。这些发现为AC在调节肠道微生物组中的作用提供了强有力的证据。介导胆汁酸代谢，这对于阻止结肠癌的进展至关重要。版权所有 © 2024 Wang、Zhu、Hua、Sun、Tan、Chang、Tang 和 Gu。

Alterations in the gut microbiome and bile acid metabolism are known to play a role in the development and progression of colon cancer. Medicinal plants like Astragalus mongholicus Bunge and Curcuma aromatica Salisb. (AC) have shown preferable therapeutic effect on cancer therapy, especially digestive tract tumors like colon cancer. However, the precise mechanisms of AC inhibiting colon cancer, particularly in relation to the gut microbiome and bile acid dynamics, are not fully understood.Our research aimed to investigate the anti-tumor properties of AC in mice with CT26 colon cancer and further investigate its underlying mechanism via intestinal microbiota. The size and pathological changes of solid tumors in colon cancer are used to evaluate the inhibitory effect of AC on colon cancer. Metagenomics and 16s rRNA gene sequencing were employed to clarify the dysbiosis in the gut microbiome of colon cancer and its impact on colon cancer. The levels of bile acids (BAs) in the feces of mice from each group were measured using UPLC-Qtrap-MS/MS.AC effectively suppressed the growth of colon cancer and reduced histological damage. Notably, AC treatment led to changes in the gut microbiome composition, with a decrease in pathogenic species like Citrobacter and Candidatus_Arthromitus, and an increase in beneficial microbial populations including Adlercreutzia, Lachnospiraceae_UCG-001, and Parvibacter. Additionally, AC altered bile acid profiles, resulting in a significant decrease in pro-carcinogenic bile acids such as deoxycholic acid (DCA) and lithocholic acid (LCA), while increasing the concentration of the cancer-inhibitory bile acid, ursodeoxycholic acid (UDCA). Tracking and analyzing the data, AC may mainly upregulate FabG and baiA genes by increasing the relative abundance of Adlercreutzia and Parvibacter bacteria, which promoting the metabolism of pro-carcinogenic LCA.These findings provide strong evidence supporting the role of AC in regulating gut microbiome-mediated bile acid metabolism, which is crucial in impeding the progression of colon cancer.Copyright © 2024 Wang, Zhu, Hua, Sun, Tan, Chang, Tang and Gu.