Evidence map›Paper›PMID 29568918›Full record

ArticleMolecular medicine reports2018

Protection of Luteolin-7-O-glucoside against apoptosis induced by hypoxia/reoxygenation through the MAPK pathways in H9c2 cells.

Shenjie Chen, Bingsheng Yang, Yifei Xu, Yiqing Rong, Yuangang Qiu

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
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  3. LC-HRMS/MS-Guided Profiling and Biological Evaluation ofMolecules (Basel, Switzerland) · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Shenjie ChenDepartment of Cardiology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006, P.R. China.
Bingsheng YangDepartment of Cardiology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006, P.R. China.
Yifei XuDepartment of Cardiology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006, P.R. China.
Yiqing RongDepartment of Cardiology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006, P.R. China.
Yuangang QiuDepartment of Cardiology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006, P.R. China.
Zhejiang Chinese Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial hypertrophy is often associated with myocardial infarction. Luteolin-7-O-glucoside (LUTG) has the prosperity of preventing cardiomyocyte injury. The current study aimed to explore the potential protective effect of LUTG and its relevant mechanisms in the heart. To establish the cardiac hypertrophy model in vitro, Angiotensin II (Ang II) was used to stimuli H9c2 cells in this study. The CCK‑8 assay showed that LUTG pretreatment improved cell viability of cardiomyocytes co‑treated with Ang II and ischemia/reperfusion. LUTG decreased the reactive oxygen species levels. Furthermore, it was demonstrated LUTG could reduce the release amount of lactate dehydrogenase and recover the catalase activity according to the flow cytometry analysis, and activity detection, respectively in Ang II‑H/R‑treated H9c2 cells. In addition, the flow cytometry analysis showed that the pretreatment of LUTG mitigated cell apoptosis induced by hypoxia/reoxygenation in the cardiac hypertrophy model. Meanwhile, reverse transcription‑quantitative polymerase chain reaction and western blot assays showed that the apoptosis‑related genes, including poly (ADP‑ribose) polymerase, Fas, Fasl and Caspase‑3 were downregulated at the transcriptional and translational levels. Notably, the protien expression of phosphorylated (p)‑extracellular signal‑regulated kinas (ERK) 1/2, p‑janus kinase and p‑P38 were reduced, while the expression of p‑ERK5 was elevated in the LUTG pretreatment groups compared with the hypoxia/reoxygenation treatment group. Based on these results, it was suggested that the anti‑apoptosis effect of LUTG may be associated with regulating the activation of mitogen‑activated protein kinases signaling pathways.

Indexed as

AnimalsApoptosisCardiomegalyCardiotonic AgentsCell HypoxiaCell LineFlavonesGlucosidesLuteolinMAP Kinase Signaling SystemMyocardial Reperfusion InjuryMyocytes, CardiacPhosphorylationRatsCardiotonic AgentsFlavonesGlucosidesLuteolinluteolin-7-glucosideapoptosisLuteolin-7-O-glucosideMAPKsreactive oxygen species

Identifiers

PMID29568918
PMCPMC5928668
OpenAlexW2790195297

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.