Evidence map›Paper›PMID 25122164›Full record

ArticlePloS one2014

Qishenyiqi protects ligation-induced left ventricular remodeling by attenuating inflammation and fibrosis via STAT3 and NF-κB signaling pathway.

Chun Li, Yong Wang, Qi Qiu, Tianjiao Shi, Yan Wu, Jing Han, Xingyun Chai, Wei Wang

Abstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  13. Yang-xin-xue keli exerts therapeutic effectsFrontiers in pharmacology · 2022
    Article
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  17. QiShenYiQi Pill Improves Myocardial Hypertrophy Caused by Pressure Overload in Rats.Evidence-based complementary and alternative medicine : eCAM · 2021
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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.

Chun LiModern Research Center for Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Yong WangBasic Medical College, Beijing University of Chinese Medicine, Beijing, China.
Qi QiuAnzhen Hospital of Capital Medical University, Beijing, China.
Tianjiao ShiBasic Medical College, Beijing University of Chinese Medicine, Beijing, China.
Yan WuBasic Medical College, Beijing University of Chinese Medicine, Beijing, China.
Jing HanBasic Medical College, Beijing University of Chinese Medicine, Beijing, China.
Xingyun ChaiModern Research Center for Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Wei WangBasic Medical College, Beijing University of Chinese Medicine, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimQi-shen-yi-qi (QSYQ), a formula used for the routine treatment of heart failure (HF) in China, has been demonstrated to improve cardiac function through down-regulating the activation of the Renin-Angiotensin-Aldosterone System (RAAS). However, the mechanisms governing its therapeutic effects are largely unknown. The present study aims to demonstrate that QSYQ treatment can prevent left ventricular remodeling in heart failure by attenuating oxidative stress and inhabiting inflammation.

methodsSprague-Dawley (SD) rats were randomly divided into 6 groups: sham group, model group (LAD coronary artery ligation), QSYQ group with high dosage, middle dosage and low dosage (LAD ligation and treated with QSYQ), and captopril group (LAD ligation and treated with captopril as the positive drug). Indicators of fibrosis (Masson, MMPs, and collagens) and inflammation factors were detected 28 days after surgery.

resultsResults of hemodynamic alterations (dp/dt value) in the model group as well as other ventricular remodeling (VR) markers, such as MMP-2, MMP-9, collagen I and III elevated compared with sham group. VR was accompanied by activation of RAAS (angiotensin II and NADPHoxidase). Levels of pro-inflammatory cytokines (TNF-α, IL-6) in myocardial tissue were also up-regulated. Treatment of QSYQ improved cardiac remodeling through counter-acting the aforementioned events. The improvement of QSYQ was accompanied with a restoration of angiotensin II-NADPHoxidase-ROS-MMPs pathways. In addition, "therapeutic" QSYQ administration can reduce both TNF-α-NF-B and IL-6-STAT3 pathways, respectively, which further proves the beneficial effects of QSYQ.

conclusionsOur study demonstrated that QSYQ protected LAD ligation-induced left VR via attenuating AngII -NADPH oxidase pathway and inhabiting inflammation. These findings provide evidence as to the cardiac protective efficacy of QSYQ to HF and explain the beneficial effects of QSYQ in the clinical application for HF.

Indexed as

Angiotensin IIAnimalsCaptoprilDrugs, Chinese HerbalFibrosisHeart FailureHeart VentriclesHemodynamicsInflammationInterleukin-6LigationMaleMatrix MetalloproteinasesNADPH OxidasesNF-kappa BOxidative StressAngiotensin IICaptoprilDrugs, Chinese HerbalInterleukin-6Matrix MetalloproteinasesNADPH OxidasesNF-kappa BProtective AgentsReactive Oxygen SpeciesStat3 protein, ratSTAT3 Transcription Factor

Identifiers

PMID25122164
PMCPMC4133204

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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.