ArticleJournal of molecular histology2026
Parthenolide attenuates sepsis-associated coagulopathy by suppressing NR3C2 in endothelial cells.
Article in Journal of molecular histology, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the protective effects of parthenolide (PTL) in sepsis-associated coagulopathy (SAC) and its underlying molecular mechanisms.
methodsA mouse model of sepsis was generated to evaluate PTL's effects on lung histopathological changes, inflammatory factor expression, and coagulation dysfunction. In HMEC-1 cells, the impact of PTL on lipopolysaccharide (LPS)-induced inflammation, procoagulant state, and apoptosis was analyzed. Bioinformatics analysis was employed to predict PTL's target genes. These predicted targets were cross-referenced with sepsis and coagulation dysfunction-associated genes for key regulators. The expression changes of the key candidate, Nuclear receptor subfamily 3 group C member 2 (NR3C2), were validated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR), immunohistochemistry (IHC), and Western blot. Molecular docking analysis was subsequently performed to predict the potential interaction between PTL and NR3C2. Furthermore, an NR3C2 overexpression experiment was conducted to investigate its functional role in the protective effects mediated by PTL.
resultsPTL pretreatment attenuated lung histopathological damage and reduced the levels of inflammatory cytokines and coagulation-related markers, including tissue factor (TF), plasminogen activator inhibitor-1 (PAI-1), and thrombin-antithrombin complex (TAT), in septic mice. In HMEC-1 cells, PTL effectively suppressed LPS-induced inflammation, procoagulant activity, and apoptosis. Bioinformatics analysis, corroborated by experimental validation, suggested that NR3C2 might be a key target of PTL. Molecular docking analysis further demonstrated a favorable binding affinity between PTL and NR3C2. NR3C2 overexpression partially reversed the PTL-induced reductions in inflammatory responses and cellular injury, suggesting that NR3C2 may be involved in these effects of PTL.
conclusionPTL attenuates selected coagulation-related abnormalities and inflammatory injury in experimental sepsis, and these effects may be associated with the regulation of NR3C2 expression. These findings provide preliminary evidence supporting further investigation of PTL and NR3C2 in sepsis-associated coagulopathy (SAC).
Indexed as
Identifiers
42611381What 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.