Evidence map›Paper›PMID 33174139›Full record

ArticleInflammation2021

Memantine, NMDA Receptor Antagonist, Attenuates ox-LDL-Induced Inflammation and Oxidative Stress via Activation of BDNF/TrkB Signaling Pathway in HUVECs.

Ying Hao, Rui Xiong, Xue Gong

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Review
  2. Review
  3. Hepatocyte BDNF Acts as a Novel Immune Checkpoint to Restrain TLR4-Mediated Acute Hepatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Article
  5. Article
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  7. Protective Effect ofJournal of microbiology and biotechnology · 2025
    Article
  8. Review
  9. Article
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  15. 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

3 authors.

Ying Hao *Department of Cardiology, Shanghai East Hospital, Tongji University, 1800 Yuntai Rd, Shanghai, 200126, People's Republic of China. ljil602d@163.com.ORCID http://orcid.org/0000-0002-0314-7118
Rui Xiong *Department of Cornea, Affiliated Eye Hospital of Nanchang University, 463 Bayi Avenue, Nanchang City, 330006, Jiangxi Province, People's Republic of China. rxiong3@uic.edu.
Xue GongDepartment of Cardiology, DeltaHealth Hospital, Shanghai, 201702, People's Republic of China.

Funding

Key Disciplines Group Construction Project of Pudong Health Bureau of Shanghai No. PWZxq2017-05the Top-level Clinical Discipline Project of Shanghai Pudong No. PWYgf2018-02
6 · The paper itself

Abstract

Atherosclerosis is a chronic cardiovascular disease and contributes to pathogenesis of most myocardial infarction and ischemic stroke. Additionally, N-methyl-D-aspartate (NMDA) receptor plays a crucial role in myocardial infarction and ischemic strokes. The aim of our study was to investigate the underlying mechanisms of memantine (MEM), the blocker of NMDA receptors, in the development of atherosclerosis. In our study, human umbilical vascular endothelial cells (HUVECs) were stimulated with low-density lipoprotein (ox-LDL) to establish an atherosclerotic cell model. Cell Counting Kit-8 (CCK-8) assay and TUNEL staining were performed to detect the cell activity and apoptosis of HUVECs, respectively. The levels of inflammatory cytokines and malondialdehyde and the activities of lactate dehydrogenase (LDH), superoxide dismutase (SOD), and caspase-1 were quantified with commercial assay kits. Finally, qRT-PCR assay and western blot analysis were carried out to determine the mRNA and protein expressions of inflammation-related genes in HUVECs. The results of the present study suggested that ox-LDL stimulation induced decreased viability of HUVECs, excessive inflammation, and oxidative stress, while these effects were counteracted by MEM treatment. Interestingly, MEM triggered the activation of BDNF/TrkB signaling pathway in HUVECs, and K252a, the inhibitor of the BDNF/TrkB pathway, abolished the suppressive effect of MEM on ox-LDL-induced inflammation, oxidative stress, and apoptosis in HUVECs. Overall, MEM attenuated ox-LDL-induced inflammation, oxidative stress, and apoptosis via activation of BDNF/TrkB signaling pathway in HUVECs, indicating that MEM may be defined as a novel and effective agent for atherosclerosis treatment.

Indexed as

ApoptosisAtherosclerosisBiomarkersBlotting, WesternBrain-Derived Neurotrophic FactorCells, CulturedCytokinesEnzyme-Linked Immunosorbent AssayExcitatory Amino Acid AntagonistsHumansHuman Umbilical Vein Endothelial CellsInflammationIn Situ Nick-End LabelingLipoproteins, LDLMemantineMembrane GlycoproteinsBDNF protein, humanBiomarkersBrain-Derived Neurotrophic FactorCytokinesExcitatory Amino Acid AntagonistsLipoproteins, LDLMemantineMembrane Glycoproteinsoxidized low density lipoproteinReceptors, N-Methyl-D-AspartateReceptor, trkBtropomyosin-related kinase-B, humanatherosclerosisinflammationmemantineN-methyl-D-aspartate (NMDA) receptoroxidative stress

Identifiers

What OpenQuestion holds

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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.