ArticleFrontiers in pharmacology2025
Parishin E from ginger-processed
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- Exosomal delivery of METTL3 promotes M1 macrophage polarization by inducing miR-155-5p maturation via m6A modification.Annals of medicine · 2026Article
- The emerging role of lactate in skeletal homeostasis and disorders: Integrated mechanisms and translational opportunities.Journal of orthopaedic translation · 2026Review
- Review
- Metabolic-epigenetic rewiring in rheumatoid arthritis: from pathogenic memory to precision restoration.Frontiers in immunology · 2026Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: This study investigated the natural small molecule drug Parishin E (PE) derived from the orchid plant Methods: An Sprague-Dawley rat model of rheumatoid arthritis was constructed to evaluate the pharmacological effects of G-GEB. Plant non-targeted metabolomics, serum non-targeted metabolomics, and RAW264.7 inflammation models elucidate Parishin E as the core anti-inflammatory component of G-GEB. Subsequently, transcriptomic and metabolomic analyses were performed to elucidate the molecular signaling mechanism of Parishin E in the treatment of RA. Results: G-GEB significantly improves RA, with 363 active compounds identified by untargeted metabolomics. PE, its main active component, affects cell glycolysis by downregulating HK2 and LDHA to inhibit macrophage polarization. PE also shows anti-inflammatory properties by suppressing H3 lactylation at H3K18la and H3K27la. Conclusion: PE in G-GEB exerts an RA ameliostatic effect by inhibiting macrophage polarization by regulating cellular glycolysis and by inhibiting the emulsylation modification of histone H3 sites, specifically H3K18la and H3K27la. Therefore, PE is a promising drug candidate for the development of RA treatments.
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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 Socratic graph.