Evidence map›Paper›PMID 31842027›Full record

ArticleCoronary artery disease2020

Tanshinone IIA protects mice against atherosclerotic injury by activating the TGF-β/PI3K/Akt/eNOS pathway.

Junyan Wang, Xinyong He, Wenna Chen, Ni Zhang, Junfu Guo, Jingjing Liu, Lin Zhang, Hongwei Sun, Lianqun Jia, Guanlin Yang

Open access · hybridAbstract read
In one paragraph

Article in Coronary artery disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 22 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

10 authors at 1 institution in 2 countries.

Junyan WangKey Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications.
Xinyong HeKey Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications.
Wenna ChenDepartment of Medical Science of Laboratory.
Ni ZhangKey Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications.
Junfu GuoDepartment of Medical Science of Laboratory.
Jingjing LiuKey Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications.
Lin ZhangBasic Medical College, Liaoning University of Traditional Chinese Medicine, Shenyang, Liaoning, China.
Hongwei SunKey Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications.
Lianqun JiaKey Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications.
Guanlin YangKey Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications.
Liaoning University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveExplored the mechanism of action of tanshinone IIA (TIIA) against atherosclerosis.

methodsApoE mice were divided into two groups of 10: model and TIIA. A control group of 10 wild-type mice was created. ApoE mice were fed a high-fat diet for 12 weeks. The TIIA group received TIIA once daily. Mice were anesthetized, blood collected by cardiac puncture, and the aortic sinus/arch collected for histology and molecular studies, respectively.

resultsMice intima in the model group had large areas of plaque formation, serum levels of total cholesterol (TC), triglycerides, and low-density lipoprotein-cholesterol (LDL-C) increased significantly, and high-density lipoprotein-cholesterol (HDL-C) levels decreased significantly in the model group after 12 weeks. Staining [hematoxylin and eosin (H&E), Oil-Red-O] showed that the aorta had lesions, a higher degree of plaque formation, and considerable lipid deposition in model-group mice. After TIIA treatment, expression of HDL-C was increased significantly and that of TC, triglycerides and LDL-C decreased significantly, and plaque size and lipid deposition improved obviously. Analyses of protein phosphorylation in aortic tissue suggested that the transforming growth factor (TGF)-β/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/endothelial nitric oxide synthase (eNOS) pathway was activated in TIIA-treated mice.

conclusionTIIA can lower levels of serum lipids, stabilize atherosclerotic plaques, reduce endothelial injury, and inflammatory damage by activation of the TGF-β/PI3K/Akt/eNOS pathway.

Indexed as

AbietanesAnimalsAorta, ThoracicAtherosclerosisBiomarkersDisease Models, AnimalEnzyme-Linked Immunosorbent AssayImmunosuppressive AgentsMaleMiceMice, Inbred C57BLMice, KnockoutNitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionAbietanesBiomarkersImmunosuppressive AgentsNitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akttanshinoneTransforming Growth Factor beta

Identifiers

PMID31842027
PMCPMC7192539
OpenAlexW2996087208

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.