Mechanism of Banxia Houpo Decoction in Treating Gastroesophageal Reflux Disease: An Integrated Approach of Compound Analysis, Network Pharmacology and Empirical Verification.
10.1007/s11655-025-3825-x
- Author:
Shun-Zhe SONG
1
;
Jiang-Nan XIE
1
;
Jing-Wen ZHANG
1
;
Ai-Xia GONG
2
Author Information
1. Digestive Endoscopy, the First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, 116000, China.
2. Digestive Endoscopy, the First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, 116000, China. doctorgax@sina.com.
- Publication Type:Journal Article
- Keywords:
Banxia Houpo Decoction;
gastroesophageal reflux disease;
lower esophageal sphincter;
network pharmacology;
serotonin transporter
- MeSH:
Animals;
Gastroesophageal Reflux/physiopathology*;
Drugs, Chinese Herbal/chemistry*;
Rats, Sprague-Dawley;
Network Pharmacology;
Male;
Serotonin/metabolism*;
Rats;
Disease Models, Animal;
Serotonin Plasma Membrane Transport Proteins/metabolism*;
Esophagus/drug effects*
- From:
Chinese journal of integrative medicine
2025;31(10):889-898
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To elucidate the mechanism of Banxia Houpo Decoction (BHD) in treating gastroesophageal reflux disease (GERD) by integrating and utilizing the compound analysis, network pharmacology, and empirical verification.
METHODS:Ultra-high performance liquid chromatography-high resolution mass spectrometry (UPLC-HRMS) was utilized to identify the primary compounds in BHD. Network pharmacology was employed to retrieve target genes. A GERD rat model was developed and 32 SD rats were randomly divided into model, BHD-L (3 g/kg), BHD-H (6 g/kg), and mosapride (0.75 mg/kg) groups using a random number table, 8 rats in each group. Eight rats without the construction of a GERD model were selected as the blank group. Esophageal damage was evaluated through visualization and histopathology evaluation. 5-hydroxytryptamine (5-HT) levels in serum and lower esophageal sphincter (LES) were determined by ELISA. LES contractility was measured with a force transducer, and serotonin transporter (SERT) and 5-HT4R expressions in LES were assessed by RT-PCR, Western blot, and immunofluorescence staining, respectively.
RESULTS:UPLC-HRMS analysis identified 37 absorption peaks and 157 compounds in BHD. Functional enrichment identified SERT as a significant target for LES contractility. Histopathological findings indicated less severe esophageal mucosal damage in the BHD-H group compared with the model group. Although serum 5-HT levels showed no significant difference, 5-HT concentration in LES tissue was notably higher in the BHD-H group (P<0.05). Within the range from 10-10 to 10-7 mmol/L, LES contractility in the BHD-H and mosapride groups was significantly increased (P<0.05). Within the range from 3 × 10-7 to 3 × 10-6 mmol/L 5-HT, LES contractility in the BHD-H group was increased (P<0.05). No significant difference was detected within the range from 10-5 to 10-4 mmol/L 5-HT. Notably, SERT expression in the BHD-H group assessed by RT-PCR, Western blot, and immunofluorescence staining were significantly lower than that in the model group (all P<0.01); while 5-HT4R expression remained unchanged.
CONCLUSION:BHD may increase LES contractility by inhibiting SERT expression in LES tissue.
