Evidence map›Paper›PMID 26035532›Full record

ArticleInternational journal of molecular medicine2015

Nicorandil protects mesenchymal stem cells against hypoxia and serum deprivation-induced apoptosis.

Fengyun Zhang, Jinjin Cui, Bo Lv, Bo Yu

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.8field-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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Nicorandil reduces the antimicrobial effectiveness of polymyxin E againstFrontiers in cellular and infection microbiology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Fengyun ZhangKey Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, P.R. China.
Jinjin CuiKey Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, P.R. China.
Bo LvKey Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, P.R. China.
Bo YuKey Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, P.R. China.
Harbin Medical University · CNSecond Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nicorandil, an adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channel opener, has been shown to exert a significant protective effect against ischemic heart injury. In the present study, we investigated the anti-apoptotic effects of nicorandil on rat mesenchymal stem cells (MSCs) subjected to hypoxia and serum deprivation (H/SD), as well as the potential underlying mechanisms. Apoptosis was induced in the MSCs by exposure to H/SD, and the apoptotic rates and reactive oxygen species (ROS) levels were determined by flow cytometry. The mitochondrial inner membrane potential was measured using the membrane-permeable dye, JC-1. Western blot analysis was used to measure the levels of Akt, Bcl-2, Bax, cytochrome c and cleaved caspase-3. The cell proliferative ability was assessed using the cell counting kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assay. The results revealed that H/SD-induced apoptosis was significantly attenuated by treatment with nicorandil in a concentration-dependent manner. Moreover, nicorandil markedly reduced the levels of ROS which were induced by exposure to H/SD, and increased the stability of mitochondrial membrane potential and the Bcl-2/Bax ratio, while it concomitantly decreased the H/SD-induced cleavage of caspase-3 and the release of cytochrome c. Treatment with the phosphoinositide 3-kinase (PI3K) inhibitor, LY294002, abolished the beneficial effects of nicorandil on the MSCs. In conclusion, the findings of the present study indicate that nicorandil exerts protective effects against MSC apoptosis induced by H/SD and that these effects are mediated through the PI3K/Akt, mitochondrial and ROS signaling pathways.

Indexed as

AnimalsApoptosisCell HypoxiaCell ProliferationCells, CulturedEnzyme ActivationKATP ChannelsMesenchymal Stem CellsNicorandilPhosphatidylinositol 3-KinasesProtective AgentsProto-Oncogene Proteins c-aktRats, Sprague-DawleyReactive Oxygen SpeciesSerumSignal TransductionKATP ChannelsNicorandilPhosphatidylinositol 3-KinasesProtective AgentsProto-Oncogene Proteins c-aktReactive Oxygen Species

Identifiers

PMID26035532
PMCPMC4501655
OpenAlexW2101042911

What OpenQuestion holds

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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.