ArticleCombinatorial chemistry & high throughput screening2026
Formononetin Alleviates MNNG-Triggered Chronic Atrophic Gastritis: Its Potential Mechanisms.
Article in Combinatorial chemistry & high throughput screening, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
introductionChronic atrophic gastritis (CAG) is the initial phase in the carcinogenesis of gastric cancer (GC). Therefore, effective treatment for CAG is important in reducing the risk of GC progression. As an isoflavone compound, formononetin (FMN) has been identified as a potential therapeutic agent for acute gastric ulcers and GC. However, no study has reported the protective effect of FMN against CAG and its underlying mechanism. This study aimed to explore the therapeutic effects of FMN on CAG and its underlying mechanisms
methodsNetwork pharmacology was applied to predict the core targets of FMN therapy in CAG. The CAG cell model was developed using N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-triggered human gastric epithelial cells (GES-1). The CCK-8 assay was applied to estimate cellular viability. The expression of inflammatory cytokines in cell supernatant was detected by ELISA. The protein levels and localization of nuclear receptor coactivator 1 (NCOA1), c-Jun, and c-Fos were evaluated using western blotting and immunofluorescence staining. Cell apoptosis was measured using flow cytometry.
resultsNetwork pharmacology analysis identified c-Jun as the core target of FMN in the treatment of CAG, with biological processes primarily involving the regulation of apoptosis and inflammation. DISCUSSION: This study employed network pharmacology analysis to identify FMN's therapeutic targets for CAG and validated the underlying mechanisms in vitro. While these results are promising, in vivo validation is required to confirm the efficacy of FMN. A comparative pharmacological evaluation against existing therapeutic agents and bioactive compounds would further elucidate FMN's therapeutic potential for CAG treatment.
conclusionFMN ameliorated the cell damage that MNNG triggered in GES-1 cells. The mechanism involved the anti-inflammatory and anti-apoptotic effects of FMN via modulation of the NCOA1/AP-1 signaling axis. The present preliminary study found FMN to exhibit a potential therapeutic effect against CAG.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.