Evidence map›Paper›PMID 32377729›Full record

ArticleMolecular medicine reports2020

Ginkgolide B inhibits hydrogen peroxide‑induced apoptosis and attenuates cytotoxicity via activating the PI3K/Akt/mTOR signaling pathway in H9c2 cells.

Jin Liu, Peng Wu, Zhihui Xu, Jun Zhang, Jiabao Liu, Zhijian Yang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

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  15. Antioxidants (Basel, Switzerland) · 2022
    Review
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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.

Jin LiuDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Peng WuDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Zhihui XuDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Jun ZhangDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Jiabao LiuDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Zhijian YangDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Jiangsu Province Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ginkgolide B (GB) is a diterpene lactone found in the leaves of the traditional Chinese medicinal plant Ginkgo that has been shown to have various pharmacological effects. However, the anti‑apoptotic properties of GB in cardiovascular disease remain poorly understood. The present study aimed to investigate the effect of GB on hydrogen peroxide‑induced cell injury in cardiac H9c2 cells, and to further clarify its protective mechanism of action. An in vitro hydrogen peroxide‑treated H9c2 cell model was used in order to mimic myocardial ischemia‑reperfusion (I/R) injury. Cell viability was assessed by the Cell Counting Kit‑8 assay. The induction of apoptosis was determined by flow cytometry and staining was performed using Hoechst 33342. In addition, the effect of GB on the expression levels of apoptosis‑associated proteins was evaluated by western blot analysis. The present study demonstrated that GB protected against hydrogen peroxide‑induced cytotoxicity and cell apoptosis in H9c2 cardiac cells. GB upregulated the expression level of the anti‑apoptotic protein Bcl‑2 and downregulated the expression levels of the pro‑apoptotic proteins cleaved caspase‑3 and Bax in hydrogen peroxide‑treated H9c2 cells. The molecular mechanism underlying the anti‑apoptotic effects of GB was subsequently detected. GB pretreatment activated the PI3K/Akt/mTOR signaling pathway and caused an increase in the phosphorylation levels of Akt and mTOR in hydrogen peroxide‑treated H9c2 cells. These results revealed that GB inhibited hydrogen peroxide‑induced apoptosis in H9c2 cells via activation of the PI3K/Akt/mTOR signaling pathway. These findings indicate the potential therapeutic benefits of GB in the treatment of myocardial I/R injury.

Indexed as

AnimalsApoptosisCardiotonic AgentsCell LineCell SurvivalGinkgolidesHydrogen PeroxideLactonesMyocardial Reperfusion InjuryMyocytes, CardiacPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsSignal TransductionTOR Serine-Threonine KinasesCardiotonic Agentsginkgolide BGinkgolidesHydrogen PeroxideLactonesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinasescell apoptosisGinkgolide Bmyocardial ischemia/reperfusion injuryoxidative stressphosphatidyl inositol 3 kinase/protein kinase B/mammalian target of rapamycin

Identifiers

PMID32377729
PMCPMC7248522
OpenAlexW3023670739

What OpenQuestion holds

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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.