Evidence map›Paper›PMID 27399653›Full record

ArticleMolecules (Basel, Switzerland)2016

Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes.

Bin Zhang, Yaping Chen, Qiang Shen, Guiyan Liu, Jingxue Ye, Guibo Sun, Xiaobo Sun

Abstract 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
–field-weighted citation impact
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.

  1. Review
  2. Review
  3. Article
  4. Review
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  6. Review
  7. Article
  8. Article
  9. Review
  10. Guan Xin Dan Shen formulation protectsMolecular medicine reports · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Flavonoids: From Structure to Health Issues.Molecules (Basel, Switzerland) · 2017
    Article
  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

7 authors.

Bin ZhangInstitute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100193, China. zhangbin7@126.com.
Yaping ChenSchool of Life Science, Beijing Institute of Technology, Beijing 100081, China. Yp_chen@yeah.net.
Qiang ShenCenter of Research and Development on Life Sciences and Environmental Sciences, Harbin University of Commerce, Harbin 150076, China. jinqilinsq@163.com.
Guiyan LiuSchool of Life Science, Beijing Institute of Technology, Beijing 100081, China. gyliu@bit.edu.cn.
Jingxue YeInstitute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100193, China. yejingxue2002@126.com.
Guibo SunInstitute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100193, China. sunguibo@126.com.
Xiaobo SunInstitute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100193, China. sunsubmit@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperglycemia, as well as diabetes mellitus, has been shown to trigger cardiac cell apoptosis. We have previously demonstrated that myricitrin prevents endothelial cell apoptosis. However, whether myricitrin can attenuate H9c2 cell apoptosis remains unknown. In this study, we established an experiment model in H9c2 cells exposed to high glucose. We tested the hypothesis that myricitrin may inhibit high glucose (HG)-induced cardiac cell apoptosis as determined by TUNEL staining. Furthermore, myricitrin promoted antioxidative enzyme production, suppressed high glucose-induced reactive oxygen species (ROS) production and decreased mitochondrial membrane potential (MMP) in H9c2 cells. This agent significantly inhibited apoptotic protein expression, activated Akt and facilitated the transcription of NF-E2-related factor 2 (Nrf2)-mediated protein (heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO-1) expression as determined by Western blotting. Significantly, an Akt inhibitor (LY294002) or HO-1 inhibitor (ZnPP) not only inhibited myricitrin-induced HO-1/NQO-1 upregulation but also alleviated its anti-apoptotic effects. In summary, these observations demonstrate that myricitrin activates Nrf2-mediated anti-oxidant signaling and attenuates H9c2 cell apoptosis induced by high glucose via activation of Akt signaling.

Indexed as

ApoptosisSignal TransductionAnimalsAntioxidantsCell LineFlavonoidsGlucoseHeme Oxygenase-1HyperglycemiaMitochondria, HeartModels, BiologicalMyocytes, CardiacNF-E2-Related Factor 2Oxidative StressPhosphatidylinositol 3-KinasesPlant ExtractsAntioxidantsFlavonoidsGlucoseHeme Oxygenase-1myricitrinNF-E2-Related Factor 2Phosphatidylinositol 3-KinasesPlant ExtractsProto-Oncogene Proteins c-aktReactive Oxygen SpeciesapoptosisH9c2 cellhyperglycemiaoxidative stressreactive oxygen species

Identifiers

PMID27399653
PMCPMC6274128

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Registered trials

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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.