ArticleMolecular biology reports2026
Panax notoginseng saponins (PNS)alleviates rheumatoid arthritis by regulating HIF-1α/PKM2-mediated glycolysis to inhibit Th17 differentiation.
Article in Molecular biology reports, 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
7 authors.
Funding
Abstract
purposeTo assess Panax notoginseng saponins(PNS)'s therapeutic potential against RA and its modulation of Th17 differentiation, specifically the in vitro mechanism by which PNS inhibits Th17 cell glycolysis via the HIF-1α pathway.
methodsCollagen-induced arthritis (CIA) mouse model was established by immunization with type II collagen. CIA mice were randomly divided into control, model, and PNS (100 mg/kg) treatment groups. Network pharmacology was employed to identify PNS active components and RA-related targets; protein-protein interaction (PPI) network construction and pathway enrichment analysis were used to predict core targets. Naive CD4⁺T cells were induced to differentiate into Th17 cells with interleukin (IL)-6, IL-23, and transforming growth factor-β (TGF-β), and treated with PNS at concentrations of 5, 10, and 20 µg/mL). Th17 differentiation, IL-17 A secretion, and pathway-related molecules were detected by flow cytometry, ELISA, RT-qPCR, and immunoblotting. Compound 3 K and DFOM validated the mechanism.
resultsPNS attenuated CIA severity (reduced hind paw swelling, arthritis scores, improved body weight, alleviated pathology). KEGG linked Th17 differentiation, PKM2, HIF-1α to PNS's anti-RA effects. PNS reduced Th17 ratios, inhibited PKM2/HIF-1α expression, suppressed PKM2-mediated glycolysis, and reversed HIF-1α hyperactivation in Th17 cells.
conclusionsPNS relieves CIA by inhibiting Th17 differentiation via suppressing HIF-1α-mediated PKM2 expression and glycolysis-dependent Th17 differentiation.
Indexed as
Identifiers
42429989What OpenQuestion 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 OpenQuestion graph.