Evidence map›Paper›PMID 26881030›Full record

ArticleOxidative medicine and cellular longevity2016

Polydatin Attenuates H2O2-Induced Oxidative Stress via PKC Pathway.

Huilian Qiao, Hao Chen, Yuhang Dong, He Ma, Guangchao Zhao, Fakuan Tang, Zhen Li

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. The Invasive SpeciesFrontiers in pharmacology · 2022
    Pooled it
  2. PKCδ regulates the vascular biology in diabetic atherosclerosis.Cell communication and signaling : CCS · 2023
    Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Polydatin Attenuates Neuronal LossFrontiers in pharmacology · 2019
    Article
  9. Polydatin Alleviates Radiation-Induced Testes Injury by Scavenging ROS and Inhibiting Apoptosis Pathways.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

7 authors at 2 institutions in 1 country.

Huilian QiaoDepartment of Histology and Embryology, The Fourth Military Medical University, Xi'an 710032, China.ORCID 0000-0003-3163-2134
Hao ChenDepartment of Cardiovascular Center, The 309th Hospital of Chinese PLA, Beijing 100193, China.ORCID 0000-0002-2057-6432
Yuhang DongDepartment of Histology and Embryology, The Fourth Military Medical University, Xi'an 710032, China.ORCID 0000-0003-1950-4594
He MaDepartment of Histology and Embryology, The Fourth Military Medical University, Xi'an 710032, China.ORCID 0000-0002-8429-8769
Guangchao ZhaoDepartment of Histology and Embryology, The Fourth Military Medical University, Xi'an 710032, China.ORCID 0000-0002-0764-7056
Fakuan TangDepartment of Cardiovascular Center, The 309th Hospital of Chinese PLA, Beijing 100193, China.ORCID 0000-0003-0434-7135
Zhen LiDepartment of Histology and Embryology, The Fourth Military Medical University, Xi'an 710032, China.ORCID 0000-0000-0172-5419
Air Force Medical University · CNThe 309th Hospital of Chinese People's Liberation Army · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress plays an important role in the pathogenesis of endothelial dysfunction, which is found to precede the development of diverse cardiovascular diseases (CVDs). The aim of this study was to observe the protective effects of PD against H2O2-induced oxidative stress injury (OSI) in human umbilical vein endothelial cells (HUVECs) and the possible mechanism of PD in OSI treatment. HUVECs were subjected to H2O2 in the absence or presence of PD. It turned out that PD improved cell viability and adhesive and migratory abilities, inhibited the release of lactate dehydrogenase (LDH) and reactive oxygen species (ROS), and elevated the content of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD). TUNEL, fluorometric assays, and Western blotting showed that OSI upregulated the apoptosis ratio, the activity of caspase-3 and the level of proapoptotic protein Bax and decreased the level of antiapoptotic protein Bcl-2. However, PD treatment partially reversed these damage effects and Protein Kinase C (PKC) activation by thymeleatoxin (THX) in turn eliminated the antiapoptotic effect of PD. Furthermore, PD attenuated the H2O2-induced phosphorylation of PKCs α and δ and increased the phosphorylation of PKC ε. Our results indicated that PD might exert protective effects against OSI through various interactions with PKC pathway.

Indexed as

Hydrogen PeroxideOxidative StressApoptosisDrugs, Chinese HerbalGlucosidesHumansHuman Umbilical Vein Endothelial CellsProtein Kinase CSignal TransductionStilbenesDrugs, Chinese HerbalGlucosidesHydrogen PeroxidepolydatinProtein Kinase CStilbenes

Identifiers

PMID26881030
PMCPMC4736317
OpenAlexW2230650976

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.