Evidence map›Paper›PMID 26499405›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2015

Niclosamide inhibits the inflammatory and angiogenic activation of human umbilical vein endothelial cells.

Mingcheng Huang, Qian Qiu, Shan Zeng, Youjun Xiao, Maohua Shi, Yaoyao Zou, Yujin Ye, Liuqin Liang, Xiuyan Yang, Hanshi Xu

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
0.5field-weighted citation impact, top 33% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.

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  10. A dual-action niclosamide-based prodrug that targets cancer stem cells and inhibits TNBC metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2023
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  11. Injectable niclosamide nanohybrid as an anti-SARS-CoV-2 strategy.Colloids and surfaces. B, Biointerfaces · 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

10 authors at 2 institutions in 1 country.

Mingcheng Huang
Qian Qiu
Shan Zeng
Youjun Xiao
Maohua Shi
Yaoyao Zou
Yujin Ye
Liuqin Liang
Xiuyan Yang
Hanshi Xu
The First Affiliated Hospital, Sun Yat-sen University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveNiclosamide is known to have anti-cancer and anti-inflammatory activities; however, its therapeutic mechanism has not been defined. In this study, to explain the therapeutic mechanism of niclosamide, we examined the effect of niclosamide on endothelial cell activation,leukocyte integration, proliferation, migration and angiogenesis in vitro.

methodsEndothelia-leukocyte adhesion assays were used to assess primary cultures of human umbilical vein endothelial cells’ (HUVECs) activation following TNF-α treatment. Each step of angiogenesis was evaluatedin vitro, including endothelial cell proliferation, migration and tube formation. Proliferation was examined using EdU assays, while wound migration assays and transwell assays were used to evaluate cell migration; cord like structure formation assays on Matrigel were used to assess tube formation. In vivo matrigel plug assay was used to assess angiogenesis. The protein expression was measured using western blot.

resultsNiclosamide reduced the adhesion of human monocyte cells to HUVECs. Niclosamide also reduced protein expression of VCAM-1 and ICAM1 in HUVECs.Niclosamide significantly inhibited HUVEC proliferation,migration and cord-like structure formation. Niclosamide also suppresses VEGF-induced angiogenesis in vivo.Niclosamide attenuated IKK-mediated activation of NF-κB pathway in TNFα-induced endothelial cells. Niclosamide also suppresses VEGF-induced endothelial VEGFR2 activation and downstream P-AKT, P-mTOR and P-p70S6K.

conclusionsNiclosamide exerted a potent effect on HUVECs activation, suggesting that it might function via an endothelia-based mechanism in the treatment of various diseases, including rheumatoid arthritis and cancer.

Indexed as

Angiogenesis Inducing AgentsAnti-Inflammatory AgentsCell MovementCell ProliferationHumansHuman Umbilical Vein Endothelial CellsIntercellular Adhesion Molecule-1LeukocytesNeovascularization, PathologicNiclosamideTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1Vascular Endothelial Growth Factor AWound HealingAngiogenesis Inducing AgentsAnti-Inflammatory AgentsIntercellular Adhesion Molecule-1NiclosamideTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1Vascular Endothelial Growth Factor A

Identifiers

PMID26499405
OpenAlexW2258796509

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.