Evidence map›Paper›PMID 29538428›Full record

ArticlePloS one2018

Cardioprotection of tilianin ameliorates myocardial ischemia-reperfusion injury: Role of the apoptotic signaling pathway.

Cheng Zeng, Wen Jiang, Ruifang Zheng, Chenghui He, Jianguang Li, Jianguo Xing

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  5. Review
  6. Article
  7. Article
  8. Article
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  10. Article
  11. Review
  12. Tilianin Reduces ApoptosisFrontiers in pharmacology · 2022
    Article
  13. Article
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  15. Article
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  18. Observational
  19. Review
  20. Tilianin Extracted FromFrontiers in pharmacology · 2020
    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.

Cheng ZengCollege of Pharmacy, Xinjiang Medical University, Urumqi, Xinjiang, P.R. China.
Wen JiangDepartment of Pharmacy, The Sixth Affiliated Hospital, Xinjiang Medical University, Urumqi, Xinjiang, P.R. China.
Ruifang ZhengCollege of Pharmacy, Xinjiang Medical University, Urumqi, Xinjiang, P.R. China.
Chenghui HeXinjiang Institute of Materia Medica, Urumqi, Xinjiang P.R. China.
Jianguang LiCollege of Pharmacy, Xinjiang Medical University, Urumqi, Xinjiang, P.R. China.
Jianguo XingXinjiang Institute of Materia Medica, Urumqi, Xinjiang P.R. China.ORCID 0000-0002-5711-5664
Xinjiang Medical University · CNXinjiang Institute of Materia Medica · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous research demonstrated that tilianin protects the myocardium in a myocardial ischemia reperfusion injury (MIRI) rat model and has prominent pharmacological potential as a cardiovascular drug. Our study aimed to investigate the molecular signaling implicated in the improvement of myocardial survival induced by tilianin, a flavonoid antioxidant. Tilianin (2.5, 5, and 10 mg/kg/d) or saline was orally administered to rats for 14 days. On the 15th day, ischemia was induced by ligating the left anterior descending artery for 45 min, followed by 4 h of reperfusion. The levels of MIRI-induced serum myocardial enzymes and cardiomyocyte apoptosis as well as infarct size were examined to assess the cardioprotective effects. Cardiac tissues were collected for western blot analyses to determine the protein expression of anti-apoptotic signaling molecules. In MIRI-treated rats, our results revealed that pre-administration of high dose-tilianin the reduced release of LDH, MDA, and CK-MB and increased the plasma SOD level, and significantly attenuated the infarct size. Western blot analysis showed that a remarkable rise in expression of Bcl-2 and XIAP, and decline in expression of Bax, Smac/Diablo, HtrA2/Omi, cleaved caspase-3, caspase-7 and caspase-9 was observed in the myocardium. The apoptosis index of cardiomyocytes further supports the cardioprotective effect of tilianin. Additionally, compared with the MIRI model group, pretreatment with high dose-tilianin group upregulated phosphorylated Akt and PI3K. In contrast, using the PI3K inhibitor LY294002 to block Akt activation effectively inhibited the protective effects of tilianin against MIRI. Tilianin pretreatment was beneficial for activating the PI3K/Akt signaling pathway and inhibiting myocardial apoptosis.

Indexed as

Administration, OralAnimalsApoptosisCardiotonic AgentsChromonesDisease Models, AnimalDose-Response Relationship, DrugDrugs, Chinese HerbalEnzyme InhibitorsFlavonoidsGlycosidesMaleMolecular StructureMorpholinesMyocardial Reperfusion InjuryMyocytes, Cardiac2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneCardiotonic AgentsChromonesDrugs, Chinese HerbalEnzyme InhibitorsFlavonoidsGlycosidesMorpholinesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akttilianin

Identifiers

PMID29538428
PMCPMC5851616
OpenAlexW2793225477

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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.