Evidence map›Paper›PMID 27007368›Full record

ArticleMolecules (Basel, Switzerland)2016

Isoquercitrin Inhibits Hydrogen Peroxide-Induced Apoptosis of EA.hy926 Cells via the PI3K/Akt/GSK3β Signaling Pathway.

Meixia Zhu, Jiankuan Li, Ke Wang, Xuliang Hao, Rui Ge, Qingshan Li

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 51 citations in OpenAlex.

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  9. Soluble epoxide hydrolase (Archives of medical science : AMS · 2021
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  11. Review
  12. The Protective Effect of DiDang Tang Against AlClFrontiers in pharmacology · 2020
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  17. Article
  18. Review
  19. Article
  20. 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

6 authors at 2 institutions in 1 country.

Meixia ZhuDepartment of Pharmacy Shanxi, College of Traditional Chinese Medicine, No. 121 University Avenue, Taiyuan 030619, China. meixiaz032@163.com.
Jiankuan LiSchool of Pharmaceutical Science, Shanxi Medical University, No. 56 Xinjian South Road, Taiyuan 030001, China. lijiankuan2004@163.com.
Ke WangDepartment of Pharmacy Shanxi, College of Traditional Chinese Medicine, No. 121 University Avenue, Taiyuan 030619, China. wangk1758@163.com.
Xuliang HaoShanxi Province Academy of Traditional Chinese Medicine, No. 46 Bingzhou West Road, Taiyuan 030012, China. hxliang-01@163.com.
Rui GeSchool of Pharmaceutical Science, Shanxi Medical University, No. 56 Xinjian South Road, Taiyuan 030001, China. cpugr@126.com.
Qingshan LiSchool of Pharmaceutical Science, Shanxi Medical University, No. 56 Xinjian South Road, Taiyuan 030001, China. sxlqs2012@163.com.
Shanxi Medical University · CNShanxi Province Hospital of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress plays a critical role in endothelial injury and the pathogenesis of diverse cardiovascular diseases, including atherosclerosis. Isoquercitrin (quercetin-3-glucoside), a flavonoid distributed widely in plants, exhibits many biological activities, including anti-allergic, anti-viral, anti-inflammatory, and anti-oxidative effects. In the present study, the inhibitory effect of isoquercitrin on H2O2-induced apoptosis of EA.hy926 cells was evaluated. MTT assays showed that isoquercitrin significantly inhibited H2O2-induced loss of viability in EA.hy926 cells. Hoechst33342/PI and Annexin V-FITC/PI fluorescent double staining indicated that isoquercitrin inhibited H2O2-induced apoptosis of EA.hy926 cells. Western blotting demonstrated that isoquercitrin prevented H2O2-induced increases in cleaved caspase-9 and cleaved caspase-3 expression, while increasing expression of anti-apoptotic protein Mcl-1. Additionally, isoquercitrin significantly increased the expression of p-Akt and p-GSK3β in a dose-dependent manner in EA.hy926 cells. LY294002, a PI3K/Akt inhibitor, inhibited isoquercitrin-induced GSK3β phosphorylation and increase of Mcl-1 expression, which indicated that regulation of isoquercitrin on Mcl-1 expression was likely related to the modulation of Akt activation. These results demonstrated that the anti-apoptotic effect of isoquercitrin on H2O2-induced EA.hy926 cells was likely associated with the regulation of isoquercitrin on Akt/GSK3β signaling pathway and that isoquercitrin could be used clinically to interfere with the progression of endothelial injury-associated cardiovascular disease.

Indexed as

ApoptosisCell SurvivalChromonesEndothelial CellsGene Expression RegulationGlycogen Synthase Kinase 3 betaHumansHydrogen PeroxideMorpholinesOncogene Protein v-aktOxidative StressPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsQuercetinSignal Transduction2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesGlycogen Synthase Kinase 3 betaHydrogen PeroxideisoquercitrinMorpholinesOncogene Protein v-aktPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsQuercetinapoptosisEA.hy926 cellsisoquercitrinoxidative stressPI3K/Akt/GSK3β

Identifiers

PMID27007368
PMCPMC6273854
OpenAlexW2300446561

What OpenQuestion holds

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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.