Evidence map›Paper›PMID 28922345›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2017

Tilianin Post-Conditioning Attenuates Myocardial Ischemia/Reperfusion Injury via Mitochondrial Protection and Inhibition of Apoptosis.

Yangyang Wang, Yong Yuan, Xinchun Wang, Yanfang Wang, Jiang Cheng, Li Tian, Xinhong Guo, Dongmei Qin, Wenjiang Cao

Open access · bronzeAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.3field-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

12 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Tilianin Reduces ApoptosisFrontiers in pharmacology · 2022
    Article
  6. Review
  7. Article
  8. Article
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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 2 institutions in 1 country.

Yangyang WangFirst Affiliated Hospital of The Medical College, Shihezi University, Shihezi, Xinjiang, China (mainland).
Yong YuanFirst Affiliated Hospital of The Medical College, Shihezi University, Shihezi, Xinjiang, China (mainland).
Xinchun WangFirst Affiliated Hospital of The Medical College, Shihezi University, Shihezi, Xinjiang, China (mainland).
Yanfang WangFirst Affiliated Hospital of The Medical College, Shihezi University, Shihezi, Xinjiang, China (mainland).
Jiang ChengFirst Affiliated Hospital of The Medical College, Shihezi University, Shihezi, Xinjiang, China (mainland).
Li TianFirst Affiliated Hospital of The Medical College, Shihezi University, Shihezi, Xinjiang, China (mainland).
Xinhong GuoFirst Affiliated Hospital of The Medical College, Shihezi University, Shihezi, Xinjiang, China (mainland).
Dongmei QinPharmacy of College, Shihezi University, Shihezi, Xinjiang, China (mainland).
Wenjiang CaoFirst Affiliated Hospital of The Medical College, Shihezi University, Shihezi, Xinjiang, China (mainland).
First Affiliated Hospital of Shihezi University Medical College · CNShihezi University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND The aim of this study was to investigate the role of tilianin in modulating mitochondrial functions and mitochondria-mediated apoptosis during cardio-protection. MATERIAL AND METHODS Myocardial ischemia/reperfusion (I/R) injury was induced by 30 minutes coronary occlusion followed by two hours reperfusion in Sprague-Dawley rats. To investigate the cardio-protective effects of tilianin, apoptosis was evaluated by TUNEL. Mitochondrial ultrastructure and function were assessed by transmission electron microscopy, dynamics of mitochondrial permeability transition pore (mPTP) opening and ATP production in the myocardium; Ca2+ content and reactive oxygen species (ROS) were measured to evaluated the level of damage factors in the mitochondria. The related apoptotic proteins were analyzed through immunoblot. RESULTS Pretreatment with tilianin significantly reduced apoptosis after I/R injury in rats (p<0.05). In addition, tilianin could alleviate mitochondrial damage, markedly inhibited mPTP opening and improved ATP production (p<0.05). There was also a significant reduction for content of Ca2+ and ROS in the mitochondria (p<0.01). Apoptosis protein analysis found that treatment with tilianin led to the downregulation of apoptosis-inducing factor (AIF) (p<0.01), and suppressed the leakage of cytochrome c and activation of caspase-3 (p<0.05). CONCLUSIONS This study showed that tilianin can alleviate apoptosis of cardiomyocytes and protect myocardium, possibly via the protection of mitochondria and repression of mitochondrial apoptotic pathways. Mechanistically, inhibition of Ca2+ overload, mPTP opening, and ROS production in mitochondria may explain the observed tilianin-mediated treatment effects.

Indexed as

AnimalsApoptosisCardiotonic AgentsFlavonoidsGlycosidesMaleMembrane Potential, MitochondrialMitochondriaMitochondria, HeartMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardial IschemiaMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacRatsCardiotonic AgentsFlavonoidsGlycosidesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreReactive Oxygen Speciestilianin

Identifiers

PMID28922345
PMCPMC5614336
OpenAlexW2756204538

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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.