Evidence map›Paper›PMID 27398138›Full record

ArticleAmerican journal of translational research2016

JNK/PI3K/Akt signaling pathway is involved in myocardial ischemia/reperfusion injury in diabetic rats: effects of salvianolic acid A intervention.

Qiuping Chen, Tongda Xu, Dongye Li, Defeng Pan, Pei Wu, Yuanyuan Luo, Yanfeng Ma, Yang Liu

Open access · greenAbstract read
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 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 58 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

8 authors at 1 institution in 1 country.

Qiuping ChenInstitute of Cardiovascular Disease Research, Xuzhou Medical University 84 West Huaihai Road, Xuzhou, Jiangsu, People's Republic of China.
Tongda XuDepartment of Cardiology, Affiliated Hospital of Xuzhou Medical University 99 West Huaihai Road, Xuzhou 221002, Jiangsu, People's Republic of China.
Dongye LiInstitute of Cardiovascular Disease Research, Xuzhou Medical University84 West Huaihai Road, Xuzhou, Jiangsu, People's Republic of China; Department of Cardiology, Affiliated Hospital of Xuzhou Medical University99 West Huaihai Road, Xuzhou 221002, Jiangsu, People's Republic of China.
Defeng PanInstitute of Cardiovascular Disease Research, Xuzhou Medical University 84 West Huaihai Road, Xuzhou, Jiangsu, People's Republic of China.
Pei WuInstitute of Cardiovascular Disease Research, Xuzhou Medical University 84 West Huaihai Road, Xuzhou, Jiangsu, People's Republic of China.
Yuanyuan LuoDepartment of Cardiology, Affiliated Hospital of Xuzhou Medical University 99 West Huaihai Road, Xuzhou 221002, Jiangsu, People's Republic of China.
Yanfeng MaDepartment of Cardiology, Affiliated Hospital of Xuzhou Medical University 99 West Huaihai Road, Xuzhou 221002, Jiangsu, People's Republic of China.
Yang LiuInstitute of Cardiovascular Disease Research, Xuzhou Medical University 84 West Huaihai Road, Xuzhou, Jiangsu, People's Republic of China.
Xuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have demonstrated that diabetes impairs the phosphatidylinositol 3-kinase/Akt (PI3K/Akt) pathway, while insulin resistance syndrome has been associated with alterations of this pathway in diabetic rats after ischemia/reperfusion (I/R), and activation of C-jun N-terminal kinase (JNK) is involved. The present study was designed to investigate whether inhibiting JNK activity would partially restore the PI3K/Akt signaling pathway and protect against myocardial I/R injury in diabetic rats, and to explore the effect of intervention with salvianolic acid A (Sal A). The inhibitor of JNK (SP600125) and Sal A were used in type 2 diabetic (T2D) rats, outcome measures included heart hemodynamic data, myocardial infarct size, the release of lactate dehydrogenase (LDH), SERCA2a activity, cardiomyocyte apotosis, expression levels of Bcl-2, Bax and cleaved caspase-3, and the phosphorylation status of Akt and JNK. The p-Akt levels were increased after myocardial I/R in non-diabetic rats, while there was no change in diabetic rats. Pretreatment with the SP600125 and Sal A decreased the p-JNK levels and increased the p-Akt levels in diabetic rats with I/R, and heart hemodynamic data improved, infarct size and LDH release decreased, SERCA2a activity increased, Bax and cleaved caspase-3 expression levels decreased, and the expression of Bcl-2 and the Bcl-2/Bax ratio increased. Our results suggest that the JNK/PI3K/Akt signaling pathway is involved in myocardial I/R injury in diabetic rats and Sal A exerts an anti-apoptotic effect and improves cardiac function following I/R injury through the JNK/PI3K/Akt signaling pathway in this model.

Indexed as

Diabetic ratsischemia/reperfusionJNKPI3K/Akt signaling pathwaySal A

Identifiers

PMID27398138
PMCPMC4931149
OpenAlexW2505645431

What OpenQuestion holds

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Read underepoch 390

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.