ArticleFrontiers in pharmacology2026
Celastrol ameliorates ulcerative colitis by inhibiting HSP90-mediated necroptosis of intestinal epithelial cells.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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
- Erratum issued
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by intestinal barrier dysfunction and epithelial cell death. Necroptosis of intestinal epithelial cells (IECs) mediated by the RIPK1/RIPK3/MLKL pathway has emerged as a key driver of UC progression. Celastrol, a bioactive compound from Celastrus wilfordii, has shown anti-inflammatory potential, but its effect on necroptosis in UC remains unclear. Methods: A dextran sulfate sodium (DSS)-induced UC mouse model and a TSZ-induced HT-29 cell necroptosis model were established. Disease activity, colon length, histology, mucus barrier integrity, and tight junction protein expression were evaluated. Western blotting, immunofluorescence, qRT-PCR, and a cellular thermal shift assay (CESTA) were used to assess necroptosis and potential targeting of HSP90. Results: Celastrol significantly improved body weight, disease activity index, and colon length, while restoring mucus secretion and tight junction proteins (ZO-1, Occludin, Muc-2). It reduced phosphorylation of RIPK1, RIPK3, and MLKL both in vivo and in vitro, decreased pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), and attenuated TUNEL-positive IEC death. CESTA indicated that celastrol increased HSP90 thermal stability, suggesting HSP90 engagement. Discussion: Celastrol ameliorates DSS-induced colitis by inhibiting HSP90-mediated necroptosis of intestinal epithelial cells, supporting its potential as a candidate for UC therapy.
Indexed as
Identifiers
What 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.