Published online Jun 15, 2026. doi: 10.4251/wjgo.v18.i6.119130
Revised: February 10, 2026
Accepted: March 12, 2026
Published online: June 15, 2026
Processing time: 141 Days and 1.5 Hours
Gastric cancer (GC) remains a leading cause of cancer mortality worldwide. Despite improved survival with surgery combined with chemotherapy and im
To establish a Simulator of the Human Intestinal Microbial Ecosystem (SHIME) model for explicitly elucidating the segment-specific metabolism of PMT.
Using the SHIME model, this study simulated the absorption of PMT in GC pa
Components of PMT were converted into small-molecule phenolic acids by microbiota. Their absorption and metabolism showed heterogeneity and dynamics across intestinal segments, e.g., flavonoid glycosides are activated rapidly in the small intestine, while hydrophobic terpenes are retained in the colon. The shifted primary absorption site in the intervention group (e.g., epicatechin from the small intestine in the control group to the colon in the treatment group) suggests that dysbiosis may reshape drug absorption pathways, providing a theoretical basis for natural nutrient-based nutritional strategies for cancer patients.
The SHIME model revealed PMT’s metabolism-repair dual pathway in chemotherapy and immunotherapy-damaged intestines, laying a theoretical foundation for its targeted nutritional rehabilitation strategies for cancer patients’ intestinal microecology.
Core Tip: This study established an intestinal microbial ecosystem (Simulator of the Human Intestinal Microbial Ecosystem) model to uncover the differential absorption and metabolism profiles of Premna microphylla Turcz. (PMT) across various intestinal segments. We demonstrated that chemotherapy-induced gut microbiota dysbiosis leads to a shift in the primary absorption site of active ingredients toward the colon. These findings not only provide a scientific basis for developing novel strategies to improve cancer patient prognosis but also lay a solid theoretical foundation for utilizing PMT as a low-toxicity therapeutic agent.