Evidence map›Paper›PMID 32811965›Full record

ArticleActa pharmacologica Sinica2021

Betulinic acid hydroxamate prevents colonic inflammation and fibrosis in murine models of inflammatory bowel disease.

María E Prados, Adela García-Martín, Juan D Unciti-Broceta, Belén Palomares, Juan A Collado, Alberto Minassi, Marco A Calzado, Giovanni Appendino, Eduardo Muñoz

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.2field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. RELA Ablation Contributes to Progression of Hepatocellular Carcinoma with TP53Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  4. Cerium single-atom catalysts-armedActa pharmaceutica Sinica. B · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
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  12. Prospective therapeutics for intestinal and hepatic fibrosis.Bioengineering & translational medicine · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Revisiting fibrosis in inflammatory bowel disease: the gut thickens.Nature reviews. Gastroenterology & hepatology · 2022
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

María E PradosEmerald Health Biotechnology, Cordoba, Spain.
Adela García-MartínEmerald Health Biotechnology, Cordoba, Spain.
Juan D Unciti-BrocetaEmerald Health Biotechnology, Cordoba, Spain.
Belén PalomaresMaimonides Biomedical Research Institute of Cordoba, Cordoba, Spain.
Juan A ColladoMaimonides Biomedical Research Institute of Cordoba, Cordoba, Spain.
Alberto MinassiDepartment of Drug Science, University of Piemonte Oriental, Novara, Italy.
Marco A CalzadoMaimonides Biomedical Research Institute of Cordoba, Cordoba, Spain.
Giovanni AppendinoDepartment of Drug Science, University of Piemonte Oriental, Novara, Italy.
Eduardo MuñozMaimonides Biomedical Research Institute of Cordoba, Cordoba, Spain. fi1muble@uco.es.
Instituto Maimónides de Investigación Biomédica de Córdoba · ESUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITUniversity of Córdoba · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal fibrosis is a common complication of inflammatory bowel disease (IBD) and is defined as an excessive accumulation of scar tissue in the intestinal wall. Intestinal fibrosis occurs in both forms of IBD: ulcerative colitis and Crohn's disease. Small-molecule inhibitors targeting hypoxia-inducing factor (HIF) prolyl-hydroxylases are promising for the development of novel antifibrotic therapies in IBD. Herein, we evaluated the therapeutic efficacy of hydroxamate of betulinic acid (BHA), a hypoxia mimetic derivative of betulinic acid, against IBD in vitro and in vivo. We showed that BAH (5-20 μM) dose-dependently enhanced collagen gel contraction and activated the HIF pathway in NIH-3T3 fibroblasts; BAH treatment also prevented the loss of trans-epithelial electrical resistance induced by proinflammatory cytokines in Caco-2 cells. In two different murine models (TNBS- and DSS-induced IBD) that cause colon fibrosis, oral administration of BAH (20, 50 mg/kg·d, for 17 days) prevented colon inflammation and fibrosis, as detected using immunohistochemistry and qPCR assays. BAH-treated animals showed a significant reduction of fibrotic markers (Tnc, Col1a2, Col3a1, Timp-1, α-SMA) and inflammatory markers (F4/80

Indexed as

AnimalsAnti-Inflammatory AgentsBetulinic AcidCaco-2 CellsColonDextran SulfateFibrosisGastrointestinal AgentsGene ExpressionHumansHydroxamic AcidsInflammationInflammatory Bowel DiseasesIntestinal MucosaMaleMiceAnti-Inflammatory AgentsBetulinic AcidDextran SulfateGastrointestinal AgentsHydroxamic AcidsPentacyclic TriterpenesTrinitrobenzenesulfonic Acidbetulinic acid hydroxamatecolon inflammationDSSfibrosishypoxia-inducible factorinflammatory bowel diseaseprolyl hydroxylasesTNBS

Identifiers

PMID32811965
PMCPMC8209138
OpenAlexW3050443461

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.