Evidence map›Paper›PMID 32319555›Full record

ArticleInternational journal of molecular medicine2020

Cinnamaldehyde protects against oxidative stress and inhibits the TNF‑α‑induced inflammatory response in human umbilical vein endothelial cells.

Nam-Yi Kim, Nguyet-Tran Trinh, Sang-Gun Ahn, Soo-A Kim

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.8field-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

27 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  7. Carvacrol@ZnO andMolecules (Basel, Switzerland) · 2025
    Article
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  15. The role and mechanism of cinnamaldehyde in cancer.Journal of food and drug analysis · 2024
    Review
  16. Article
  17. Cinnamon: a nutraceutical supplement for the cardiovascular system.Archives of medical sciences. Atherosclerotic diseases · 2024
    Article
  18. Article
  19. 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

4 authors at 2 institutions in 1 country.

Nam-Yi KimDepartment of Biochemistry, Dongguk University College of Oriental Medicine, Gyeongju, North Gyeongsang 38066, Republic of Korea.
Nguyet-Tran TrinhDepartment of Biochemistry, Dongguk University College of Oriental Medicine, Gyeongju, North Gyeongsang 38066, Republic of Korea.
Sang-Gun AhnDepartment of Pathology, Chosun University College of Dentistry, Gwangju 61452, Republic of Korea.
Soo-A KimDepartment of Biochemistry, Dongguk University College of Oriental Medicine, Gyeongju, North Gyeongsang 38066, Republic of Korea.
Dongguk University · KRChosun University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress and inflammation play critical roles in the development of cardiovascular diseases. Cinnamaldehyde (CA) is a natural compound from Cinnamomum cassia, and its anticancer, antimicrobial and anti‑inflammatory activities have been widely investigated. In the present study, the cytoprotective and anti‑inflammatory effects of CA on H2O2‑ or tumor necrosis factor (TNF)‑α‑exposed human umbilical vein endothelial cells (HUVECs) were examined. CA and its natural derivative, 2‑methoxycinnamaldehyde (MCA), markedly increased the cellular protein level of heme oxygenase‑1 (HO‑1) and promoted the translocation of nuclear factor erythroid 2‑related factor 2 (Nrf2) to the nucleus. CA‑mediated Nrf2/HO‑1 activation protected the HUVECs from H2O2‑induced oxidative stress, which promotes apoptosis. HO‑1 depletion by siRNA attenuated the CA‑mediated cell protective effects against oxidative stress. Additionally, CA markedly inhibited the adhesion of U937 monocytic cells to HUVECs by decreasing the expression level of vascular cell adhesion protein 1 (VCAM‑1). An in vivo experiment confirmed the anti‑inflammatory effects of CA, as lipopolysaccharide (LPS)‑induced inflammatory cell infiltration was effectively inhibited by the compound. Overall, these observations suggest that CA may be used as a therapeutic agent for oxidative stress‑mediated cardiovascular diseases, such as atherosclerosis.

Indexed as

AcroleinAnimalsBlotting, WesternHeme Oxygenase-1HumansHuman Umbilical Vein Endothelial CellsInflammationMiceNF-E2-Related Factor 2Oxidative StressTumor Necrosis Factor-alphaU937 CellsVascular Cell Adhesion Molecule-1AcroleincinnamaldehydeHeme Oxygenase-1NF-E2-Related Factor 2Tumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID32319555
PMCPMC7255462
OpenAlexW3016889236

What Socratic 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 Socratic graph.