Authors
Zhiqing Yang, Fangyuan Liu, Xuemeng Sun, Jiaxin Sun, Yabing Liang, Jie Zhang, Miao Wang, Fengyi Li, Haijing Niu, Ying Wei, Ling Yang, Liya Su
Published in
Journal of ethnopharmacology. Pages 122368. Sep 18, 2026. Epub Sep 18, 2026.
Abstract
Batri-7 (BT-7) is a classic Mongolian herbal formula traditionally valued for its anti-inflammatory properties. It has been utilized within Mongolian medicine for gastrointestinal disorders and inflammatory conditions, suggesting its potential therapeutic value in inflammation-associated colorectal carcinogenesis. However, its efficacy against inflammation-associated colorectal adenoma (IACA)-the primary precursor lesion of colitis-associated colorectal cancer (CAC)-and the underlying molecular mechanisms remain poorly understood.
This study aims to systematically evaluate the efficacy and mechanism of BT-7 in suppressing progression of established IACA by integrating network pharmacology, in vivo models, and patient-derived organoids.
The chemical profile of BT-7 was characterized by Liquid chromatography-mass spectrometry (LC-MS). Network pharmacology was employed to predict potential targets and pathways. An AOM/DSS-induced CAC mouse model was used to assess in vivo efficacy, with therapeutic dosing initiated after adenoma formation. Patient-derived IACA organoids were established and treated with BT-7 to evaluate its anti-adenoma effects in vitro. Transcriptomic analyses and functional rescue experiments were conducted to elucidate the underlying mechanisms.
BT-7 treatment significantly reduced adenoma burden and curtailed the progression of pre-existing lesions in AOM/DSS mice, alleviated colitis symptoms, and reduced proliferative activity. In patient-derived adenoma organoids, BT-7 inhibited growth and induced apoptosis in a dose- and time-dependent manner. Transcriptomic analyses consistently identified the PI3K/AKT pathway as a key target of BT-7. Functional studies confirmed that BT-7 downregulated PI3K/AKT signaling and specifically upregulated the pro-apoptotic protein BAX. Rescue experiments using PI3K and AKT activators (740Y-P and SC-79) reversed BT-7-induced growth inhibition and apoptosis, whereas an AKT inhibitor (MK-2206) phenocopied the pro-apoptotic effects of BT-7.
BT-7 effectively suppresses progression of established IACA in the inflammatory context by inhibiting the PI3K/AKT signaling pathway and activating BAX-associated apoptosis. These preclinical findings demonstrate that BT-7 exerts therapeutic efficacy against established inflammation-associated colorectal adenoma, providing a mechanistic foundation for its further translational investigation.
PMID:
42759679
Bibliographic data and abstract were imported from PubMed on 19 Sep 2026.
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