Evidence map›Paper›PMID 27122190›Full record

ArticleInternational journal of molecular medicine2016

Artemisinin inhibits monocyte adhesion to HUVECs through the NF-κB and MAPK pathways in vitro.

Yue Wang, Jiatian Cao, Yuqi Fan, Yushui Xie, Zuojun Xu, Zhaofang Yin, Lin Gao, Changqian Wang

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  4. Frontiers in pharmacology · 2024
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  14. Artemisinin and its derivatives: a potential therapeutic approach for oral lichen planus.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Review
  15. Article
  16. 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

8 authors at 1 institution in 1 country.

Yue WangDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P.R. China.
Jiatian CaoDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P.R. China.
Yuqi FanDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P.R. China.
Yushui XieDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P.R. China.
Zuojun XuDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P.R. China.
Zhaofang YinDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P.R. China.
Lin GaoDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P.R. China.
Changqian WangDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P.R. China.
Shanghai Ninth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The adhesion of monocytes to human umbilical vein endothelial cells (HUVECs) plays a crucial role in the initiation of atherosclerosis. Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are two important molecules involved in the adhesion of monocytes to HUVECs. Previous studies have suggested that artemisinin, apart from an anti-malarial agent, also has other effects. In the present study, we found that artemisinin significantly decreased the adhesion of monocytes to tumor necrosis factor-α (TNF-α)-stimulated HUVECs in a dose-dependent manner and suppressed the mRNA and protein level of ICAM-1 and VCAM-1 in the TNF-α-stimulated HUVECs. In addition, the nuclear factor-κB (NF-κB) inhibitor, Bay 11-7082, and mitogen-activated protein kinase (MAPK) inhibitors (SB203580 and U0126) respectively reduced the adhesion of monocytes to TNF-α-stimulated HUVECs, and suppressed ICAM-1 and VCAM-1 expression in TNF-α stimulated HUVECs. Moreover, artemisinin impeded the activation of the NF-κB and MAPK signaling pathways. Furthermore, Bay 11-7082 significantly decreased the phosphorylation of levels extracellular signal-regulated protein kinase (ERK)1/2, p38 and c-Jun N-terminal kinase (JNK). Taken together, the findings of our study indicated that artemisinin blocked monocyte adhesion to TNF-α-stimulated to HUVECs by downregulating ICAM-1 and VCAM-1 expression in the TNF-α-stimulated HUVECs. Artemisinin may thus have potential for use in the protection against the early development of atherosclerotic lesions.

Indexed as

Anti-Inflammatory AgentsArtemisininsButadienesCell AdhesionCell LineCoculture TechniquesGene Expression RegulationHumansHuman Umbilical Vein Endothelial CellsImidazolesIntercellular Adhesion Molecule-1JNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MonocytesNF-kappa B3-(4-methylphenylsulfonyl)-2-propenenitrileAnti-Inflammatory AgentsartemisininArtemisininsButadienesICAM1 protein, humanImidazolesIntercellular Adhesion Molecule-1JNK Mitogen-Activated Protein KinasesMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-kappa BNitrilesProtein Kinase InhibitorsPyridinesSB 203580SulfonesTumor Necrosis Factor-alphaU 0126Vascular Cell Adhesion Molecule-1

Identifiers

PMID27122190
PMCPMC4866958
OpenAlexW2345058332

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.