Regulatory Effect of Huangqin Tang on Metabolic Homeostasis During Colitis-cancer Transformation in Colitis-associated Colorectal Cancer
10.13422/j.cnki.syfjx.20251909
- VernacularTitle:黄芩汤对结肠炎相关性结直肠癌结肠炎-癌转变过程中代谢稳态的调控作用
- Author:
Xingbo ZUO
1
;
Xue FENG
2
;
Caijuan ZHANG
2
;
Haifan LIU
2
;
Jianyao LIU
2
;
Bin LIU
2
;
Lin ZHU
2
;
Qiyue SUN
2
;
Dunfang WANG
2
;
Weipeng YANG
2
Author Information
1. Heilongjiang University of Chinese Medicine， Harbin 150040，China
2. Institute of Chinese Materia Medica，China Academy of Chinese Medical Sciences，Beijing 100700，China
- Publication Type:Journal Article
- Keywords:
Huangqin Tang;
inflammation-cancer transformation;
metabolomics;
inflammation;
proliferation
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2025;31(22):21-28
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the mechanism of Huangqin Tang （HQT） in regulating metabolic reprogramming during the inflammation-cancer transformation in colitis-associated colorectal cancer （CAC）. MethodsCAC mouse model was established using the carcinogen azoxymethane （AOM） combined with the inflammatory agent dextran sulfate sodium （DSS）. HQT treatment was adopted. Serum metabolomics analysis was performed at three stages （inflammation， proliferation， and tumor formation） using liquid chromatography-tandem mass spectrometry （LC-MS/MS） untargeted metabolomics coupled with multivariate statistical analysis to explore the mechanism of HQT intervention in metabolism in CAC. ResultsThe results revealed that HQT significantly reversed the disturbance of key metabolites in CAC mice. A total of 52， 67， and 45 differential metabolites were identified in the model group， compared to the normal group， during inflammation， proliferation， and tumor stages， respectively. Lactate， linoleic acid， oleic acid， elaidic acid， and betaine were characteristic metabolites persistently enriched throughout colitis-cancer transformation. Pathway enrichment analysis of differential metabolites showed that linoleic acid metabolism and arachidonic acid metabolism were the most significantly disturbed in CAC pathogenesis. The proliferation stage featured expanded amino acid metabolic networks， while the tumor stage uniquely exhibited two new pathways of nicotinate and nicotinamide metabolism and phosphoinositide metabolism. HQT exerted stage-specific regulatory effects： targeting arachidonic acid metabolism in the inflammation stage， correcting the dysregulation of choline-carnitine metabolism in the proliferation stage， and rescuing nicotinamide and tryptophan metabolic collapse in the tumor stage. ConclusionHQT exerts regulatory effects on metabolic disorders at various stages of the colitis-cancer transformation process， thereby effectively slowing the progression from colitis to cancer. The study also reveals the dynamic metabolic characteristics of colorectal "inflammation-cancer transformation，"providing new insights for research on the targeted mechanisms of traditional Chinese medicine in anti-tumor therapy based on metabolic reprogramming.
