ArticleDrug design, development and therapy2024
Integrated Approaches Revealed the Therapeutic Mechanisms of Zuojin Pill Against Gastric Mucosa Injury in a Rat Model with Chronic Atrophic Gastritis.
Article in Drug design, development and therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Qilianshupi Decoction Alleviate Epithelial-mesenchymal Transition to Treat Chronic Atrophic Gastritis.Combinatorial chemistry & high throughput screening · 2026Article
- Jiangfu Fuwei granules alleviate chronic atrophic gastritis by suppressing angiogenesis through the PI3K-AKT-HIF1α pathway.American journal of translational research · 2026Article
- Biotransformation and biological fate of magnetic iron oxide nanoparticles for biomedical research and clinical applications.Nanoscale advances · 2025Review
- Antiproliferative and pro-apoptotic effects ofFrontiers in oncology · 2025Article
- Zuojinwan ameliorates depressive-like behavior and gastrointestinal dysfunction in mice by modulating the FXR-bile acid-gut microbiota pathway.Frontiers in microbiology · 2025Article
- Yangweishu Ameliorates Chronic Atrophic Gastritis with Stomach Yin Deficiency Syndrome Through IL-6/STAT3 Signaling Pathway.Drug design, development and therapy · 2025Article
- Treating chronic atrophic gastritis: identifying sub-population based on real-world TCM electronic medical records.Frontiers in pharmacology · 2024Article
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Authors and funding
11 authors.
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Abstract
Background: The Zuojin Pill (ZJP) is widely used for treating chronic atrophic gastritis (CAG) in clinical practice, effectively ameliorating symptoms such as vomiting, pain, and abdominal distension in patients. However, the underlying mechanisms of ZJP in treating CAG has not been fully elucidated. Purpose: This study aimed to clarify the characteristic function of ZJP in the treatment of CAG and its potential mechanism. Methods: The CAG model was established by alternant administrations of ammonia solution and sodium deoxycholate, as well as an irregular diet. Therapeutic effects of ZJP on body weight, serum biochemical indexes and general condition were analyzed. HE staining and AB-PAS staining were analyzed to characterize the mucosal injury and the thickness of gastric mucosa. Furthermore, network pharmacology and molecular docking were used to predict the regulatory mechanism and main active components of ZJP in CAG treatment. RT-PCR, immunohistochemistry, immunofluorescence and Western blotting were used to measure the expression levels of apoptosis-related proteins, gastric mucosal barrier-associated proteins and PI3K/Akt signaling pathway proteins. Results: The results demonstrated that ZJP significantly improved the general state of CAG rats, alleviated weight loss and gastric histological damage and reduced the serum biochemical indicators. Network pharmacology and molecular docking found that ZJP in treating CAG by inhibiting inflammation, suppressing apoptosis, and protecting the gastric mucosal barrier via the PI3K/Akt signaling pathway. Further experiments confirmed that ZJP obviously modulated the expression of key proteins involved in gastric mucosal cell apoptosis, such as Bax, Bad, Apaf-1, cleaved-caspase-3, cleaved-caspase-9, Cytochrome C, Bcl-2, and Bcl-xl. Moreover, ZJP significantly reversed the protein expression of Occludin, ZO-1, Claudin-4 and E-cadherin. Conclusion: Our study revealed that ZJP treats CAG by inhibiting the PI3K/Akt signaling pathway. This research provided a scientific basis for the rational use of ZJP in clinical practice.
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