Evidence map›Paper›PMID 29209026›Full record

ArticleScientific reports2017

QSKL protects against myocardial apoptosis on heart failure via PI3K/Akt-p53 signaling pathway.

Hong Chang, Chun Li, Qiyan Wang, Linghui Lu, Qian Zhang, Yi Zhang, Na Zhang, Yong Wang, Wei Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.4field-weighted citation impact, top 5% 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, 52 citations in OpenAlex.

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  18. A Network Pharmacology Approach to Explore the Mechanisms of Qishen Granules in Heart Failure.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  19. Article
  20. Silence of LncRNAMolecules and cells · 2019
    Article
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

9 authors at 2 institutions in 1 country.

Hong ChangSchool of Life Sciences, Beijing University of Chinese Medicine, Bei San Huan Dong Lu 11, ChaoYang District, Beijing, 100029, China.
Chun LiModern Research Center for Traditional Chinese Medicine, Beijing University of Chinese Medicine, Bei San Huan Dong Lu 11, ChaoYang District, Beijing, 100029, China.
Qiyan WangSchool of Life Sciences, Beijing University of Chinese Medicine, Bei San Huan Dong Lu 11, ChaoYang District, Beijing, 100029, China.
Linghui LuSchool of Life Sciences, Beijing University of Chinese Medicine, Bei San Huan Dong Lu 11, ChaoYang District, Beijing, 100029, China.
Qian ZhangSchool of Life Sciences, Beijing University of Chinese Medicine, Bei San Huan Dong Lu 11, ChaoYang District, Beijing, 100029, China.
Yi ZhangSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Bei San Huan Dong Lu 11, ChaoYang District, Beijing, 100029, China.
Na ZhangModern Research Center for Traditional Chinese Medicine, Beijing University of Chinese Medicine, Bei San Huan Dong Lu 11, ChaoYang District, Beijing, 100029, China.
Yong WangSchool of Life Sciences, Beijing University of Chinese Medicine, Bei San Huan Dong Lu 11, ChaoYang District, Beijing, 100029, China. doctor_wangyong@163.com.ORCID 0000-0003-3652-8037
Wei WangBeijing University of Chinese Medicine, Bei San Huan Dong Lu 11, ChaoYang District, Beijing, 100029, China. wangwei26960@126.com.
Beijing University of Chinese Medicine · CNNorth China University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ancient traditional Chinese medicine Qishenkeli (QSKL) is widely used in the treatment of heart failure (HF) in China. Previous studies have shown that QSKL has definite effects on HF. The purpose of this study is to identify the regulation of QSKL on apoptosis and clarify the underlying mechanism. An apoptosis model of H9C2 cells was induced by oxygen-glucose deprivation/recovery (OGD/R). An animal model of HF was induced by ligation of left anterior descending (LAD) coronary artery in rat. We found that QSKL reduced intracellular ROS generation, increased mitochondrial membrane potential and protected H9C2 cells against OGD/R-induced apoptosis. In vivo results showed that QSKL administration could improve cardiac functions, decrease fibrotic area, infarct size and apoptotic rate in HF model. QSKL regulated the expressions of key apoptotic molecules, including increasing Bcl-2/Bax ratio, reducing the expressions of P53, Bax and Cleaved-caspase-3. Interestingly, QSKL also regulated the phosphorylated expressions of PI3K and Akt without significantly affecting PTEN. Taken together, the protective and anti-apoptotic effects of QSKL could be mediated partly through modulating the PI3K/Akt-P53 apoptotic pathway.

Indexed as

AnimalsApoptosisBiomarkersCell LineDrugs, Chinese HerbalHeart FailureHumansMaleMembrane Potential, MitochondrialMyoblasts, CardiacPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRats, Sprague-DawleyReactive Oxygen SpeciesSignal TransductionTumor Suppressor Protein p53BiomarkersDrugs, Chinese HerbalPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTumor Suppressor Protein p53

Identifiers

PMID29209026
PMCPMC5717266
OpenAlexW2769614877

What OpenQuestion holds

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LicenceCC BY
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.