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Updated: Jul 30, 2026

Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration
Published on: May 7, 2018
Spatial metabolomics revealed mTOR-mediated gastric epithelial repair by licorice (G. inflata) flavonoids
Yufan Wu1, Yinglin Guo1, Dehao Huang2
1School of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510515, China.
Abstract:
Licorice (Glycyrrhiza inflata Bat.) is a traditional food homologous herbal medicine in China. Licorice flavonoid (LF), a bioactive food component extracted from licorice, has demonstrated therapeutic potential against alcohol-induced gastric ulcers (GU) by promoting mucosal regeneration and suppressing apoptosis. Excessive alcohol consumption is prevalent, and gastrointestinal disorders are generally higher in drinking populations. High concentrations of alcohol result in damage to gastric mucosa, and epithelial restoration is a highly ATP-dependent process that requires a high energy supply to maintain the gastrointestinal epithelium's regeneration, absorption qualities, and barrier function. Thus, this study investigates the role of LF in modulating energy metabolism to facilitate gastric mucosal repair through the strategy of metabolomics combined with spatial metabolomics. Firstly, LF treatment ameliorated injury of gastric mucosa, reducing ulcer index by 50 %. It also markedly decreased the extent of oxidative stress and inflammatory infiltration in GU rats. Metabonomics revealed LF regulated metabolic variations that were disordered by GU. Additionally, based on spatial metabolomics, we found that disorders of glycolysis and tricarboxylic acid (TCA) cycle caused by alcohol occurred in the mucosal, submucosal, and muscle layer, and would be reversed by LF treatment. More crucially, LF modulated the mTOR pathway, a biological energy-sensing molecule, and LF increased mTOR phosphorylation by more than 2.5 times. The promotion of energy metabolism, evidenced by a 2-fold increase in ATP levels compared with GU rats, and an enhancement in glycolysis, TCA cycle, and mitochondrial complex activity, ultimately facilitated gastric mucosal repair and regeneration. As a result, LF enhanced glycolysis, TCA cycle, and mitochondrial dynamics during gastric mucosal repair via modulating the mTOR pathway, restoring epithelial barrier function, which provided a basis for the development of novel functional licorice flavonoid products.
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