International immunopharmacology · 2025
FZHWT alleviates chronic atrophic gastritis by inhibiting inflammatory pathways and promoting mucosal repair.
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Ma Xuehui, Wang Yongli, Kong Lingjing, Zhu Wen, Zhou Xin, Li Jian, Zhao Wei, Mao Xiaoyun, Tan Guangxing
Аннотация
BACKGROUND: Chronic atrophic gastritis (CAG) is a prevalent chronic digestive disorder that, through sustained inflammation, can lead to severe mucosal damage and even gastric cancer. Current treatments offer limited efficacy, whereas Fu-Zheng-Huo-Wei Decoction (FZHWT), a traditional Chinese medicine (TCM) formulation, shows promising potential in treating CAG.
PURPOSE: This study aims to identify the key active components of FZHWT and evaluate its therapeutic effects on CAG.
METHODS: UPLC-MS/MS was used to identify the bioactive compounds in FZHWT. A CAG rat model was established to assess its therapeutic effects, and transcriptome sequencing was conducted to identify key targets and mechanisms. A CAG cell model was used for validation of the transcriptomic findings, and histological techniques and molecular biology methods were employed for further validation.
RESULTS: A total of 1362 chemical components were identified in FZHWT, of which 25 are bioavailable compounds. Differential metabolite analysis revealed four key active ingredients: Nicotiflorin, Stachydrine, 5-O-p-Coumaroylquinic acid, and N-(4-oxopentyl)-acetamide. In the CAG rat model, FZHWT significantly reduced inflammation and gastric mucosal damage. Transcriptome sequencing highlighted Sema5a as a key target and revealed the involvement of several inflammatory signaling pathways. In the CAG cell model, FZHWT alleviated CAG by inhibiting inflammation and promoting gastric mucosal repair.
CONCLUSIONS: FZHWT demonstrates significant therapeutic potential in treating CAG by modulating inflammatory pathways and promoting mucosal repair. This study provides new insights into the treatment of CAG and supports the modernization of multi-component TCM formulas.
PURPOSE: This study aims to identify the key active components of FZHWT and evaluate its therapeutic effects on CAG.
METHODS: UPLC-MS/MS was used to identify the bioactive compounds in FZHWT. A CAG rat model was established to assess its therapeutic effects, and transcriptome sequencing was conducted to identify key targets and mechanisms. A CAG cell model was used for validation of the transcriptomic findings, and histological techniques and molecular biology methods were employed for further validation.
RESULTS: A total of 1362 chemical components were identified in FZHWT, of which 25 are bioavailable compounds. Differential metabolite analysis revealed four key active ingredients: Nicotiflorin, Stachydrine, 5-O-p-Coumaroylquinic acid, and N-(4-oxopentyl)-acetamide. In the CAG rat model, FZHWT significantly reduced inflammation and gastric mucosal damage. Transcriptome sequencing highlighted Sema5a as a key target and revealed the involvement of several inflammatory signaling pathways. In the CAG cell model, FZHWT alleviated CAG by inhibiting inflammation and promoting gastric mucosal repair.
CONCLUSIONS: FZHWT demonstrates significant therapeutic potential in treating CAG by modulating inflammatory pathways and promoting mucosal repair. This study provides new insights into the treatment of CAG and supports the modernization of multi-component TCM formulas.