ArticleCurrent pharmaceutical design2026
Article in Current pharmaceutical design, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- Role of Phenolic Nanocompounds in Inflammatory Disorders: Current View and Future Aspects.Current pharmaceutical design · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundStomach Heat Syndrome (SHS) arises from the excessive consumption of spicy and greasy foods, resulting in the infiltration of pathogens and increased gastric activity, ultimately culminating in gastric injury. Coptis chinensis Franch (CC), a frequently employed remedy in Traditional Chinese Medicine (TCM) for dampness elimination, fire purging, and detoxification, has been extensively utilized.
objectiveThis study aimed to explore the functional role and in-depth molecular mechanism of CC in treating SHS.
methodsThe CC Alcohol Extract (CCAE) was obtained and analyzed using HPLC. A rat model of SHS hemorrhagic lesions was established using a combination of 8% chili powder and 60% ethanol. After oral administration of CCAE, gastric histology, Myeloperoxidase (MPO), Malondialdehyde (MDA), and Superoxide Dismutase (SOD) levels were evaluated. Further, the gene expressions of Interleukin-6 (IL-6), Interleukin-1β (IL-1β), and Tumor Necrosis Factor-α (TNF-α) were assessed, respectively, using H&E staining, colorimetry, qRT-PCR, and immunohistochemistry analyses. The network pharmacology in multiple databases, transcriptome sequencing, and non-targeted metabolomic analyses were used to identify signal pathways and molecular targets. Subsequent cellular and molecular experiments were also conducted to validate the mechanisms.
resultsThe findings demonstrated that the CCAE administration effectively mitigated SHS symptoms in rats and reduced inflammatory cytokines levels and oxidative stress. Berberine (Bbr) was identified as the primary active component responsible for the anti-SHS effects of CC. Additionally, the multi-omics analysis revealed that Bbr primarily regulates amino acid metabolism, unsaturated fatty acid metabolism, the TNF signaling pathway, and the JAK-STAT signaling pathway. Furthermore, Bbr was found to inhibit the phosphorylation of JAK2, STAT3, and P65.
conclusionCC alleviated SHS-related gastric disease by suppressing inflammatory responses and enhancing gastric mucosal function through the JAK2-STAT3-NF-κB signaling pathway and amino acid metabolism, with Bbr serving as the key component.
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Identifiers
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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 OpenQuestion graph.