Evidence map›Paper›PMID 34362284›Full record

ArticlePharmaceutical biology2021

Methyl-β-cyclodextrin suppresses the monocyte-endothelial adhesion triggered by lipopolysaccharide (LPS) or oxidized low-density lipoprotein (oxLDL).

Guo Chen, Yun Zhou, Wendiao Zhang, Ying Qin, Bo Wei, Yanan Sun, Yong Chen

Open access · goldAbstract read
In one paragraph

Article in Pharmaceutical biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Impact of Methylated Cyclodextrin KLEPTOSEInternational journal of molecular sciences · 2024
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Anti-inflammatory therapy of atherosclerosis: focusing on IKKβ.Journal of inflammation (London, England) · 2023
    Review
  12. Review
  13. Article
  14. 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

7 authors at 1 institution in 1 country.

Guo ChenCollege of Life Sciences, Nanchang University, Nanchang, Jiangxi, China.
Yun ZhouCollege of Life Sciences, Nanchang University, Nanchang, Jiangxi, China.
Wendiao ZhangJiangxi Key Laboratory for Microscale Interdisciplinary Study, Institute for Advanced Study, Nanchang University, Nanchang, Jiangxi, China.
Ying QinCollege of Life Sciences, Nanchang University, Nanchang, Jiangxi, China.
Bo WeiCollege of Life Sciences, Nanchang University, Nanchang, Jiangxi, China.
Yanan SunJiangxi Key Laboratory for Microscale Interdisciplinary Study, Institute for Advanced Study, Nanchang University, Nanchang, Jiangxi, China.
Yong ChenCollege of Life Sciences, Nanchang University, Nanchang, Jiangxi, China.ORCID https://orcid.org/0000-0003-1678-1537
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextRecent studies demonstrated the anti-atherosclerotic efficacy of cyclodextrin. However, it remains unclear whether cyclodextrin exerts the anti-atherosclerotic effect via regulating monocyte-endothelial adhesion.

objectiveTo answer that question by recruiting methyl-β-cyclodextrin (MβCD) as a cyclodextrin representative. MATERIALS AND

methodsHuman umbilical vein endothelial cells (HUVECs) were not treated, or treated with 1 µg/mL liposaccharide (LPS) or 50 µg/mL oxidized low-density lipoprotein (oxLDL) for 12 h, 5 mM MβCD for 1 h, and LPS/oxLDL (1 and 50 µg/mL, respectively for 12 h) plus MβCD (5 mM for 1 h), respectively. The effects of MβCD on LPS/oxLDL-triggered monocyte-endothelial adhesion and related molecules in signalling pathways were evaluated via confocal microscopy, flow cytometry, RT-PCR, western blotting, and cell adhesion assay.

resultsMβCD with an IC

conclusionsMβCD significantly suppresses the LPS/oxLDL-triggered monocyte-endothelial adhesion by downregulating adhesion molecule expression probably via LPS-IKK-NF-κB or oxLDL-Akt-NF-κB pathway. This study demonstrates a potential mechanism of the anti-atherosclerotic efficacy of cyclodextrin from the angle of monocyte-endothelial adhesion.

Indexed as

Atherosclerosisbeta-CyclodextrinsCell AdhesionCell SurvivalHumansHuman Umbilical Vein Endothelial CellsI-kappa B KinaseIntercellular Adhesion Molecule-1LipopolysaccharidesLipoproteins, LDLMonocytesNF-kappa BProto-Oncogene Proteins c-aktSignal TransductionVascular Cell Adhesion Molecule-1AKT1 protein, humanbeta-CyclodextrinsICAM1 protein, humanI-kappa B KinaseIntercellular Adhesion Molecule-1LipopolysaccharidesLipoproteins, LDLmethyl-beta-cyclodextrinNF-kappa Boxidized low density lipoproteinProto-Oncogene Proteins c-aktVascular Cell Adhesion Molecule-1atherosclerosiscell adhesionCyclodextrins (CDs)human umbilical vein endothelial cells (HUVECs)lipid raftNF-κBTHP-1tumour

Identifiers

PMID34362284
PMCPMC8354180
OpenAlexW3187814560

What OpenQuestion holds

Textmetadata
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.