Evidence map›Paper›PMID 29548811›Full record

ArticleBiochemical pharmacology2018

Didymin prevents hyperglycemia-induced human umbilical endothelial cells dysfunction and death.

Kirtikar Shukla, Himangshu Sonowal, Ashish Saxena, Kota V Ramana

Abstract read
In one paragraph

Article in Biochemical pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.9field-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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Flavonoids with Anti-Angiogenesis Function in Cancer.Molecules (Basel, Switzerland) · 2024
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  13. [Speculation of hemoglobin ASe pu = Chinese journal of chromatography · 2021
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  15. 2'-Hydroxyflavanone prevents LPS-induced inflammatory response and cytotoxicity in murine macrophages.Toxicology in vitro : an international journal published in association with BIBRA · 2020
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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 1 institution in 1 country.

Kirtikar ShuklaDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Himangshu SonowalDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Ashish SaxenaDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Kota V RamanaDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, USA. Electronic address: kvramana@utmb.edu.
The University of Texas Medical Branch at Galveston · US

Funding

Role of Aldose Reductase in Diabetic ComplicationsR01DK104786 · NIDDK · UNIVERSITY OF TEXAS MED BR GALVESTON · PI RAMANA, KOTA VENKATA · 2015 to 2019
$2.2M
NIDDK NIH HHS R01 DK104786
6 · The paper itself

Abstract

Although didymin, a flavonoid-O-glycosides compound naturally found in the citrus fruits, has been reported to be a potent anticancer agent in the prevention of various cancers, its role in the prevention of cardiovascular complications is unclear. Most importantly, its effect in the prevention of endothelial dysfunction, a pathological process involved in the atherogenesis, is unknown. We have examined the efficacy of didymin in preventing the high glucose (HG; 25 mM)-induced human umbilical vein endothelial cells (HUVECs) dysfunction. Our results indicate that incubation of HUVECs with HG resulted in the loss of cell viability, and pre-incubation of didymin prevented it. Further, didymin prevented the HG-induced generation of reactive oxygen species (ROS) as well as lipid peroxidation product, malondialdehyde. Pretreatment of HUVECs with didymin also prevented the HG-induced decrease in eNOS and increase in iNOS expressions. Further, didymin prevented the HG-induced monocytes cell adhesion to endothelial cells, expressions of ICAM-1 and VCAM-1 and activation of NF-κB. Didymin also prevented the release of various inflammatory cytokines and chemokines in HG-treated HUVECs. In conclusion, our results demonstrate that didymin with its anti-oxidative and anti-inflammatory actions prevents hyperglycemia-induced endothelial dysfunction and death. Thus, it could be developed as a potential natural therapeutic agent for the prevention of cardiovascular complications in diabetes.

Indexed as

Cell SurvivalDose-Response Relationship, DrugFlavonoidsGlucoseGlycosidesHumansHuman Umbilical Vein Endothelial CellsMonocytesReactive Oxygen SpeciesdidyminFlavonoidsGlucoseGlycosidesReactive Oxygen SpeciesDidyminEndothelial cellsHyperglycemiaInflammationOxidative stress

Identifiers

PMID29548811
PMCPMC5960604
OpenAlexW2791661083

What OpenQuestion holds

Textmetadata
LicenceTDM
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.