To investigate the effects of Huangjin Shuangshen Decoction (HJSS) on chronic atrophic gastritis (CAG) and the underlying mechanisms of its action.
Approach:
In vivo study: CAG was induced in mice using MNNG combined with ranitidine and irregular feeding, followed by treatment with HJSS and assessment of histopathology, gastric function, inflammatory mediators, apoptosis markers, and barrier-associated molecules, with folic acid as a positive control.
In vitro study: MNNG-injured GES-1 cells were treated with HJSS-medicated serum to validate findings.
Mechanistic exploration: Integrated transcriptomic analysis, network pharmacology, and pharmacological inhibition were used to explore the mechanisms.
Key Findings:
HJSS alleviated gastric mucosal atrophy and histopathological injury.
Improved gastric functional impairment and reduced inflammatory burden were observed.
HJSS promoted recovery of gastric mucosal barrier-associated molecules, including CFTR, ZO-1, MUC5AC, Occludin, and Claudin-1.
HJSS suppressed TNF/NF-κB signaling and reduced p65 nuclear translocation.
Interpretation:
HJSS alleviates MNNG-induced CAG by reducing inflammatory injury and promoting recovery of gastric mucosal barrier features, linked to TNF/NF-κB signaling suppression and CFTR regulation.
Limitations:
The study primarily used animal models, which may not fully replicate human conditions.
Further clinical studies are needed to validate the findings.
Conclusion:
HJSS shows potential in mitigating CAG through its anti-inflammatory effects and enhancement of gastric mucosal barrier integrity.
