Evidence map›Paper›PMID 29178936›Full record

ArticleLipids in health and disease2017

Diallyl disulphide inhibits apolipoprotein(a) expression in HepG2 cells through the MEK1-ERK1/2-ELK-1 pathway.

Xiaofeng Ma, Yami Liu, Yanmei Tan, Kai Qu, Xinglan He, Hai Zhang, Zuo Wang

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. 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

7 authors at 4 institutions in 1 country.

Xiaofeng MaDepartment of Cardiology, Affiliated Nanhua Hospital of University of South China, Hengyang, 421001, China.
Yami LiuInstitute of Cardiovascular disease, Key Laboratory for Atherosclerology of Human Province, University of South China, Hengyang, 421001, China.
Yanmei TanDepartment of Pathology, Changde Vocational Technical College, Changde, 415000, China.
Kai QuInstitute of Cardiovascular disease, Key Laboratory for Atherosclerology of Human Province, University of South China, Hengyang, 421001, China.
Xinglan HeWomen and Children Healthcare Hospital of Zhu zhou, Zhuzhou, 412000, China.
Hai ZhangDepartment of Pathology, The First Affiliated Hospital of University of South China, Hengyang, 421001, China. 735236957@qq.com.
Zuo WangInstitute of Cardiovascular disease, Key Laboratory for Atherosclerology of Human Province, University of South China, Hengyang, 421001, China. smt121101@163.com.
University of South China · CNFirst Affiliated Hospital of University of South China · CNTaizhou Vocational and Technical College · CNZhuzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLipoprotein(a) [LP(a)] is implicated as a common and independent risk factor for cardiovascular diseases. The therapeutic options currently available for reducing plasma LP(a) concentrations are limited. Diallyl disulphide (DADS), the main component of garlic, regulates lipid metabolism in hepatocytes and adipocytes through ERK1/2 signalling. This study aimed to assess the effect of DADS on apolipoprotein(a) [apo(a)] in HepG2 cells. We also determined the effects of DADS on apo(a) expression and secretion in HepG2 cells as well as the underlying mechanisms.

methodsWe examined the role of DADS on apo(a) expression in HepG2 cells by treating cell with different concentrations of DADS (10, 20, 40 and 80 μg/mL) for 24 h or treating cells with 40 μg/mL DADS for 0, 6, 12, 24 and 48 h. Then we used quantitative real-time PCR to analysis apo(a) mRNA levels, used Western blot to analysis apo(a) protein levels and used enzyme-linked immunosorbent assay to test apo(a) secreted levels. To farther determined the role of DADS, we applied Transfection of small interfering RNA to knockdown ELK-1levels and applied PD98059, a specific inhibitor of ERK1/2, to block ERK1/2 signal.

resultsThe results show DADS inhibited apo(a) at both the mRNA and protein levels in HepG2 cells in a dose-dependent manner. DADS-mediated inhibition of apoa(a) expression in HepG2 cells was attenuated when the cells were cultured in medium containing PD98059 (ERK1/2 inhibitor) or were transfected with siRNAs against MEK1 or ELK-1. Overexpression of apo(a) yielded similar results.

conclusionsThis study reveals that DADS can downregulate apo(a) expression in a dose-dependent manner via the MEK-ERK12-ELK-1 pathway.

Indexed as

Allyl CompoundsApolipoproteins ABinding SitesDrug Evaluation, PreclinicalEnzyme Activationets-Domain Protein Elk-1Gene ExpressionHep G2 CellsHumansHypolipidemic AgentsMAP Kinase Kinase 1MAP Kinase Signaling SystemPhosphorylationPromoter Regions, GeneticProtein Processing, Post-TranslationalSulfidesAllyl Compoundsallyl sulfideApolipoproteins Aets-Domain Protein Elk-1Hypolipidemic AgentsMAP Kinase Kinase 1SulfidesApolipoprotein(a)Diallyl disulfideExtracellular regulated protein kinasesHepG2 cellLipoprotein(a)Mitogen-activated protein kinases

Identifiers

PMID29178936
PMCPMC5702159
OpenAlexW2770915875

What OpenQuestion holds

Textmetadata
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.