Evidence map›Paper›PMID 26168156›Full record

ArticlePloS one2015

Wedelolactone Regulates Lipid Metabolism and Improves Hepatic Steatosis Partly by AMPK Activation and Up-Regulation of Expression of PPARα/LPL and LDLR.

Yun Zhao, Lu Peng, Li-Chao Yang, Xu-Dong Xu, Wei-Jie Li, Xiu-Mei Luo, Xin Jin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. 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
7.1field-weighted citation impact, top 4% 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, 40 citations in OpenAlex.

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  16. SREBP-2, a new target of metformin?Drug design, development and therapy · 2018
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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 2 institutions in 1 country.

Yun ZhaoDepartment of Basic Medical Sciences of Medical College, Xiamen University, Xiamen, Fujian, China; Xiamen Key Laboratory of Chiral Drugs, Xiamen, Fujian, China.
Lu PengDepartment of Basic Medical Sciences of Medical College, Xiamen University, Xiamen, Fujian, China; Xiamen Key Laboratory of Chiral Drugs, Xiamen, Fujian, China.
Li-Chao YangDepartment of Basic Medical Sciences of Medical College, Xiamen University, Xiamen, Fujian, China; Xiamen Key Laboratory of Chiral Drugs, Xiamen, Fujian, China.
Xu-Dong XuDepartment of Cardiology, Zhongshan Hospital, Xiamen, Fujian, China.
Wei-Jie LiDepartment of Basic Medical Sciences of Medical College, Xiamen University, Xiamen, Fujian, China; Xiamen Key Laboratory of Chiral Drugs, Xiamen, Fujian, China.
Xiu-Mei LuoDepartment of Basic Medical Sciences of Medical College, Xiamen University, Xiamen, Fujian, China.
Xin JinDepartment of Basic Medical Sciences of Medical College, Xiamen University, Xiamen, Fujian, China; Xiamen Key Laboratory of Chiral Drugs, Xiamen, Fujian, China.
Xiamen University · CNZhongshan Hospital of Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperlipidemia is considered one of the greatest risk factors of cardiovascular diseases. We investigated the anti-hyperlipidemic effect and the underlying mechanism of wedelolactone, a plant-derived coumestan, in HepG2 cells and high-fat diet (HFD)-induced hyperlipidemic hamsters. We showed that in cultured HepG2 cells, wedelolactone up-regulated protein levels of adenosine monophosphate activated protein kinase (AMPK) and peroxisome proliferator-activated receptor-alpha (PPARα) as well as the gene expression of AMPK, PPARα, lipoprotein lipase (LPL), and the low-density lipoprotein receptor (LDLR). Meanwhile, administration of wedelolactone for 4 weeks decreased the lipid profiles of plasma and liver in HFD-induced hyperlipidemic hamsters, including total cholesterol (TC), triglycerides (TG), and low-density lipoprotein-cholesterol (LDL-C). The activation of AMPK and up-regulation of PPARα was also observed with wedelolactone treatment. Furthermore, wedelolactone also increased the activities of superoxidase dismutase (SOD) and glutathione peroxidase (GSH-Px) and decreased the level of the lipid peroxidation product malondialdehyde (MDA) in the liver, therefore decreasing the activity of alanine aminotransferase (ALT). In conclusion, we provide novel experimental evidence that wedelolactone possesses lipid-lowering and steatosis-improving effects, and the underlying mechanism is, at least in part, mediated by the activation of AMPK and the up-regulation of PPARα/LPL and LDLR.

Indexed as

Adenylate KinaseAnimalsCoumarinsCricetinaeEnzyme ActivationFatty LiverLipid MetabolismLipoprotein LipaseMesocricetusMiceReceptors, LDLUp-RegulationAdenylate KinaseCoumarinsLipoprotein LipaseReceptors, LDLwedelolactone

Identifiers

PMID26168156
PMCPMC4500417
OpenAlexW2139836728

What OpenQuestion holds

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LicenceCC BY
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.