Evidence map›Paper›PMID 37346329›Full record

ArticleHeliyon2023

Betulin and

Michael Ofori, Cynthia Amaning Danquah, Joshua Asante, Selase Ativui, Peace Doe, Alhassan Abdul-Nasir Taribabu, Isaac Newton Nugbemado, Adwoa Nkrumah Mensah

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Frontiers in medicine · 2025
    Article
  4. Article
  5. Article
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

8 authors at 2 institutions in 1 country.

Michael OforiDepartment of Pharmaceutical Science, Dr Hilla Limann Technical University, Wa, Ghana.
Cynthia Amaning DanquahDepartment of Pharmacology, Kwame Nkrumah University of Science and Technology, Ghana.
Joshua AsanteDepartment of Pharmacology, Kwame Nkrumah University of Science and Technology, Ghana.
Selase AtivuiDepartment of Pharmacology, Kwame Nkrumah University of Science and Technology, Ghana.
Peace DoeDepartment of Pharmaceutical Science, School of Pharmacy, Central University, Accra, Ghana.
Alhassan Abdul-Nasir TaribabuDepartment of Pharmacology, Kwame Nkrumah University of Science and Technology, Ghana.
Isaac Newton NugbemadoDepartment of Pharmacology, Kwame Nkrumah University of Science and Technology, Ghana.
Adwoa Nkrumah MensahDepartment of Pharmacology, Kwame Nkrumah University of Science and Technology, Ghana.
Kwame Nkrumah University of Science and Technology · GHCentral University · GH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Pulmonary fibrosis (PF) is a lung disease characterized by scaring of lung tissue that impairs lung functions. The estimated survival time of patients with pulmonary fibrosis is 3-5 years. Bleomycin (BLM) is used clinically in the treatment of Hodgkin lymphoma and testicular germ-cell tumors. Bleomycin's mechanism of action is the inhibition of DNA and protein synthesis. This happens when leukocytes induce the release of cytokines and chemokines which increase the pro-fibrotic and pro-inflammatory cytokines such as IL-6, TNF-alpha, IL-13, IL-1β and transforming growth factor-beta 1 (TGF-β). Materials and method: There was a single oropharyngeal administration of bleomycin (80 mg/kg) in mice followed by the treatment of CAE and BET after 48 h of exposure to BLM. Results: There was increased survival rate in CAE and BET treatment groups compared to the BLM induced group. There was a marked decreased in the levels of hydroxyproline, collagen I and III in the CAE and BET treatment groups compared to BLM-treated group. The treatment groups of CAE and BET significantly down regulated the levels of pro-fibrotic and pro-inflammatory cytokines concentrations such as TGF-β1, MMP9, IL-6, IL-1β and TNF-alpha compared to an increased in the BLM treated groups. The histological findings of the lungs suggested the curative effects of CAE and BET following BLM induced pulmonary fibrosis in mice, the study showed improved lung functions with wide focal area of viable alveolar spaces and few collagen fibers deposition on lungs of treatment groups. Conclusion: CAE and BET attenuated pulmonary fibrosis by down regulating pro-fibrotic and pro-inflammatory cytokines as well as improving lung function. This could be a lead in drug discovery where compounds with anti-fibrotic effects could be developed for the treatment of lung injury.

Identifiers

PMID37346329
PMCPMC10279834
OpenAlexW4379260281

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.