Evidence map›Paper›PMID 28077993›Full record

ArticleAmerican journal of translational research2016

Peroxisome proliferator-activated receptor γ (PPARγ) mediates the protective effect of quercetin against myocardial ischemia-reperfusion injury via suppressing the NF-κB pathway.

Xinyu Liu, Zhangjie Yu, Xian Huang, Yi Gao, Xiuzhi Wang, Jianmin Gu, Song Xue

Open access · greenAbstract read
PubMed Full text at PMC
In one paragraph

Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 2 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

44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Xinyu LiuDepartment of Cardiovascular Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University No. 160 Pujian Road, Shanghai 200127, China.
Zhangjie YuDepartment of Anesthesiology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University No. 160 Pujian Road, Shanghai 200127, China.
Xian HuangDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory of Tumor Microenvironment and Inflammation, School of Medicine, Shanghai Jiao Tong University No. 280 Chongqing South Road, Shanghai 200025, China.
Yi GaoDepartment of Cardiology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University No. 160 Pujian Road, Shanghai 200127, China.
Xiuzhi WangDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory of Tumor Microenvironment and Inflammation, School of Medicine, Shanghai Jiao Tong University No. 280 Chongqing South Road, Shanghai 200025, China.
Jianmin GuDepartment of Cardiovascular Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University No. 160 Pujian Road, Shanghai 200127, China.
Song XueDepartment of Cardiovascular Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University No. 160 Pujian Road, Shanghai 200127, China.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Quercetin plays an important role in myocardial ischemia and reperfusion injury (IRI). However, the underlying mechanism for the protective effect of quercetin is largely unclear. In this study, we explored the protected effects of quercetin against myocardial IRI and its molecular mechanisms. Quercetin, GW9962 (PPARγ antagonist) or PPARγ-siRNA was administered alone or in combination prior to myocardial IRI in mice or to hypoxia and reoxygenation (H/R) treatment in H9C2 cells. Infarct size was evaluated by TTC staining after reperfusion. Myocardial injury was assessed by the serum levels of AST, CK-MB, cardiac troponin T (cTnT) and LDH. Cardiac function was measured by echocardiography. Oxidative stress injury was evaluated by analyses of inducible nitric oxide synthase (iNOS), MDA, SOD and glutathione peroxidase (GSH-PX) levels and by reactive oxygen species (ROS) detection. Myocardium apoptosis was evaluated by TUNEL staining, cleaved caspase-3 and Annexin V/PI detection. Moreover, activation of the NF-κB pathway was reflected by phosphorylation of IκB (p-IκB) and nuclear translocation of NF-κB p65. We reported that pretreatment of quercetin significantly improved cardiac function, diminished myocardial injury and reduced the infarct size. Myocardium oxidative damage and apoptosis were remarkably improved by quercetin treatment in vivo and

Indexed as

ischemia-reperfusion injurymyocardiumNF-κB pathwayperoxisome proliferator-activated receptor γQuercetin

Identifiers

PMID28077993
PMCPMC5209473
OpenAlexW2982606752

What OpenQuestion holds

Textmetadata
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.