Evidence map›Paper›PMID 30720139›Full record

ArticleMolecular medicine reports2019

Rhynchophylline ameliorates myocardial ischemia/reperfusion injury through the modulation of mitochondrial mechanisms to mediate myocardial apoptosis.

Qiao-Ji Qin, Li-Qiang Cui, Peng Li, Yong-Bin Wang, Xue-Zhi Zhang, Ming-Lei Guo

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
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  5. Article
  6. Activators of Nrf2 to Counteract Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2023
    Review
  7. Celastrol and Rhynchophylline in the mitigation of simulated muscle atrophy underSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. 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

6 authors at 2 institutions in 1 country.

Qiao-Ji QinEmergency Department, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Li-Qiang CuiDepartment of Anesthesiology, Chengyang People's Hospital, Qingdao, Shandong 266109, P.R. China.
Peng LiEmergency Department, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Yong-Bin WangEmergency Department, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Xue-Zhi ZhangEmergency Department, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Ming-Lei GuoEmergency Department, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Affiliated Hospital of Qingdao University · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rhynchophylline (RP), the primary active ingredient of Uncaria rhynchophylla, has an anti‑hypertensive effect and protects against ischemia‑induced neuronal damage. The present study aimed to examine the roles and mechanisms of RP in myocardial ischemia‑reperfusion (MI/R) injury of rat cardiomyocytes. Cell viability, reactive oxygen species, mitochondrial membrane potential (MMP) and cell apoptosis were examined by a Cell Counting Kit‑8 assay and flow cytometry, respectively. An ELISA was performed to assess the expression of oxidative stress markers. Spectrophotometry was used to detect the degree of mitochondrial permeability transition pore (mPTP) openness. Western blotting and reverse transcription‑ quantitative polymerase chain reaction assays were used to evaluate the associated protein and mRNA expression, respectively. The present results demonstrated that RP increased the cell viability of MI/R‑induced cardiomyocytes, and suppressed the MI/R‑induced apoptosis of cardiomyocytes. Additionally, RP modulated the Ca2+ and MMP levels in MI/R‑induced cardiomyocytes. Furthermore, RP decreased the oxidative stress and mPTP level of MI/R‑induced cardiomyocytes. It was additionally observed that RP affected the apoptosis‑associated protein expression and regulated the mitochondrial‑associated gene expression in MI/R‑induced cardiomyocytes. In conclusion, RP ameliorated MI/R injury through the modulation of mitochondrial mechanisms. The potential effects of RP on the protection of MI/R‑induced apoptosis of cardiomyocytes suggest that RP may be an effective target for MI/R therapy.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsBiomarkersCalciumCell SurvivalGene ExpressionMatrix MetalloproteinasesMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardial Reperfusion InjuryMyocytes, CardiacOxidative StressOxindolesRatsApoptosis Regulatory ProteinsBiomarkersCalciumMatrix MetalloproteinasesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreOxindolesrhyncophylline

Identifiers

PMID30720139
PMCPMC6423601
OpenAlexW2912884535

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.