ArticleScientific reports2025
Efficacy and potential mechanisms of jatrorrhizine on MNNG-induced chronic atrophic gastritis in rats based on serological metabolomics and molecular docking.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Alkaloids Mediate Multi-Level Modulation of Gastric Carcinogenesis: From Antibacterial and Anti-Inflammatory Actions to Antitumor Effects.International journal of molecular sciences · 2026Review
- Dual-Algorithm Integration Framework Reveals Qing-Wei-Zhi-Tong's Dual Mechanisms in Chronic Gastritis.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Mechanisms and applications of N-Methyl-N'-nitro-N-nitrosoguanidine in animal tumor models: current situation and challenges.Frontiers in oncology · 2025Review
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8 authors.
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Abstract
Jatrorrhizine (JATR), a natural isoquinoline alkaloid from Coptidis Rhizoma, exhibits various pharmacological activities, including antibacterial, anti-inflammatory, and antitumor effects. While JATR is known to treat chronic gastritis, its therapeutic potential for chronic atrophic gastritis (CAG) and its underlying mechanisms are not fully understood. This study induced CAG in rats using N-Methyl-N'-nitro-N-nitrosoguanidine (MNNG) for 12 weeks through free drinking and force-feeding. Serological metabolomics identified 23 core targets of JATR related to CAG improvement. Reverse transcription-quantitative polymerase chain reaction and western blotting confirmed the involvement of these targets. Molecular docking revealed interactions between JATR and IL-1β and Caspase-3. JATR significantly alleviated gastric inflammation and atrophy, with Kyoto Encyclopedia of Genes and Genomes analysis showing enrichment in the "Nod-like receptor-related pyroptosis pathway". JATR also enhanced GES-1 cell proliferation and reduced MNNG-induced cell damage. Additionally, JATR downregulated pyroptosis-related (Gasdermin D, NLRP3, Caspase-1) and apoptosis-related (Bcl-2, Bax, Caspase-3) markers. These findings suggest that JATR may ameliorate MNNG-induced CAG by inhibiting the activation of the Nod-like receptor-related pyroptosis pathway, supporting its potential as a therapeutic intervention for CAG.
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