Evidence map›Paper›PMID 31111658›Full record

ArticleJournal of cellular and molecular medicine2019

Dihydromyricetin protects HUVECs of oxidative damage induced by sodium nitroprusside through activating PI3K/Akt/FoxO3a signalling pathway.

Xiaoying Zhang, Lifang Wang, Lizhi Peng, Xiaoying Tian, Xiaoyuan Qiu, Huan Cao, Qiaohong Yang, Rifang Liao, Fengxia Yan

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
7.3field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

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  13. The Water Extract ofAntioxidants (Basel, Switzerland) · 2023
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  17. Flavonoids-Natural Gifts to Promote Health and Longevity.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Review
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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

9 authors at 3 institutions in 1 country.

Xiaoying ZhangDepartment of Pharmacology, School of Medicine, Xizang Minzu University, Xianyang, China.
Lifang WangSchool of Medical Science, Jinan University, Guangzhou, China.
Lizhi PengDepartment of Pharmacy, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, China.
Xiaoying TianSchool of Medical Science, Jinan University, Guangzhou, China.
Xiaoyuan QiuSchool of Medical Science, Jinan University, Guangzhou, China.
Huan CaoSchool of Medical Science, Jinan University, Guangzhou, China.
Qiaohong YangSchool of Medical Science, Jinan University, Guangzhou, China.
Rifang LiaoDepartment of Pharmacy, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.ORCID 0000-0001-6454-7716
Fengxia YanSchool of Medical Science, Jinan University, Guangzhou, China.ORCID 0000-0002-8091-4384
Jinan University · CNSun Yat-sen University · CNXizang Minzu University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The damage of vascular endothelial cells induced by oxidative stress plays an important role in the pathogenesis of atherosclerosis. Dihydromyricetin (DMY) is considered as a natural antioxidant. However, the mechanism of DMY on endothelial cell injury induced by oxidative stress remains unclear. In this study, we found that DMY could reduce the oxidative damage of HUVECs induced by sodium nitroprusside (SNP), HUVECs pre-treated with DMY suppressed SNP-induced apoptosis by reduced ROS overproduction of intracellular, decreased MDA level and elevated the superoxide dismutase activity. Meanwhile, we found that DMY could promote the expression of phosphorylated FoxO3a and Akt, and affect the nuclear localization of FoxO3a, when treated with the PI3K inhibitor LY294002, the effect of DMY was blocked. These data suggest that DMY protects HUVECs from oxidative stress by activating PI3K/Akt/FoxO3a signalling pathway. Therefore, DMY may have great therapeutic potential as a new drug for atherosclerosis.

Indexed as

Cell DeathChromonesCytoprotectionFlavonolsForkhead Box Protein O3HumansHuman Umbilical Vein Endothelial CellsModels, BiologicalMorpholinesNitroprussideOxidative StressPhosphatidylinositol 3-KinasesPhosphorylationProtective AgentsProtein TransportProto-Oncogene Proteins c-akt2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesdihydromyricetinFlavonolsForkhead Box Protein O3FOXO3 protein, humanMorpholinesNitroprussidePhosphatidylinositol 3-KinasesProtective AgentsProto-Oncogene Proteins c-aktapoptosisatherosclerosisdihydromyricetinoxidative stresssodium nitroprusside

Identifiers

PMID31111658
PMCPMC6584490
OpenAlexW2946104050

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.