Evidence map›Paper›PMID 24098933›Full record

ArticleRespiratory research2013

Antiflammin-1 attenuates bleomycin-induced pulmonary fibrosis in mice.

Wei Liu, Jing Wan, Jian-Zhong Han, Chen Li, Dan-Dan Feng, Shao-Jie Yue, Yan-Hong Huang, Yi Chen, Qing-Mei Cheng, Yang Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 50 citations in OpenAlex.

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  6. Schisandrin B attenuates bleomycin-induced pulmonary fibrosis in mice through AKT-mTOR pathway.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2024
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  16. Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
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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

11 authors at 1 institution in 1 country.

Wei LiuDepartment of Physiology, Xiangya School of Medicine, Central South University, 110 Xiangya Road, Changsha 410078, PR China. luozq1962@163.com.
Jing Wan
Jian-Zhong Han
Chen Li
Dan-Dan Feng
Shao-Jie Yue
Yan-Hong Huang
Yi Chen
Qing-Mei Cheng
Yang Li
Zi-Qiang Luo
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAntiflammin-1 (AF-1), a derivative of uteroglobin (UG), is a synthetic nonapeptide with diverse biological functions. In the present study, we investigated whether AF-1 has a protective effect against bleomycin-induced pulmonary fibrosis.

methodsC57BL/6 mice were injected with bleomycin intratracheally to create an animal model of bleomycin-induced pulmonary fibrosis. On Day 7 and Day 28, we examined the anti-inflammatory effect and antifibrotic effect, respectively, of AF-1 on the bleomycin-treated mice. The effects of AF-1 on the transforming growth factor-beta 1 (TGF-β1)-induced proliferation of murine lung fibroblasts (NIH3T3) were examined by a bromodeoxycytidine (BrdU) incorporation assay and cell cycle analysis.

resultsSevere lung inflammation and fibrosis were observed in the bleomycin-treated mice on Day 7 and Day 28, respectively. Administration of AF-1 significantly reduced the number of neutrophils in the bronchoalveolar lavage fluid (BALF) and the levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) in the lung homogenates on Day 7. Histological examination revealed that AF-1 markedly reduced the number of infiltrating cells on Day 7 and attenuated the collagen deposition and destruction of lung architecture on Day 28. The hydroxyproline (HYP) content was significantly decreased in the AF-1-treated mice. In vitro, AF-1 inhibited the TGF-β1-induced proliferation of NIH3T3 cells, which was mediated by the UG receptor.

conclusionsAF-1 has anti-inflammatory and antifibrotic actions in bleomycin-induced lung injury. We propose that the antifibrotic effect of AF-1 might be related to its suppression of fibroblast growth in bleomycin-treated lungs and that AF-1 has potential as a new therapeutic tool for pulmonary fibrosis.

Indexed as

AnimalsAnti-Inflammatory AgentsBleomycinCell ProliferationDisease Models, AnimalFibroblastsHydroxyprolineInterleukin-1betaIn Vitro TechniquesLungMaleMiceMice, Inbred C57BLNIH 3T3 CellsPeptide FragmentsPulmonary Fibrosisantiflammin P1Anti-Inflammatory AgentsBleomycinHydroxyprolineInterleukin-1betaPeptide FragmentsTransforming Growth Factor beta1Tumor Necrosis Factor-alphaUteroglobin

Identifiers

PMID24098933
PMCPMC3856527
OpenAlexW2111718967

What OpenQuestion holds

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LicenceCC BY
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.