Evidence map›Paper›PMID 28146135›Full record

ArticleMolecules (Basel, Switzerland)2017

The Transcription Profile Unveils the Cardioprotective Effect of Aspalathin against Lipid Toxicity in an In Vitro H9c2 Model.

Rabia Johnson, Phiwayinkosi V Dludla, Christo J F Muller, Barbara Huisamen, M Faadiel Essop, Johan Louw

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
5.8field-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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  11. The health benefits of rooibos tea in humans (Journal of public health in Africa · 2023
    Article
  12. Review
  13. Role of Stearoyl-CoA Desaturase 1 in Cardiovascular Physiology.International journal of molecular sciences · 2023
    Review
  14. Article
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  17. Observational
  18. Article
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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

6 authors at 2 institutions in 1 country.

Rabia JohnsonBiomedical Research and Innovation Platform (BRIP), Medical Research Council (MRC), Tygerberg 7505, South Africa. rabia.johnson@mrc.ac.za.
Phiwayinkosi V DludlaBiomedical Research and Innovation Platform (BRIP), Medical Research Council (MRC), Tygerberg 7505, South Africa. pdludla@mrc.ac.za.
Christo J F MullerBiomedical Research and Innovation Platform (BRIP), Medical Research Council (MRC), Tygerberg 7505, South Africa. christo.muller@mrc.ac.za.
Barbara HuisamenBiomedical Research and Innovation Platform (BRIP), Medical Research Council (MRC), Tygerberg 7505, South Africa. bh3@sun.ac.za.
M Faadiel EssopCardio-Metabolic Research Group (CMRG), Department of Physiological Sciences, Stellenbosch University, Stellenbosch 7599, South Africa. mfessop@sun.ac.za.
Johan LouwBiomedical Research and Innovation Platform (BRIP), Medical Research Council (MRC), Tygerberg 7505, South Africa. johan.louw@mrc.ac.za.
South African Medical Research Council · ZAStellenbosch University · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aspalathin, a C-glucosyl dihydrochalcone, has previously been shown to protect cardiomyocytes against hyperglycemia-induced shifts in substrate preference and subsequent apoptosis. However, the precise gene regulatory network remains to be elucidated. To unravel the mechanism and provide insight into this supposition, the direct effect of aspalathin in an isolated cell-based system, without the influence of any variables, was tested using an H9c2 cardiomyocyte model. Cardiomyocytes were exposed to high glucose (33 mM) for 48 h before post-treatment with or without aspalathin. Thereafter, RNA was extracted and RT2 PCR Profiler Arrays were used to profile the expression of 336 genes. Results showed that, 57 genes were differentially regulated in the high glucose or high glucose and aspalathin treated groups. Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) analysis revealed lipid metabolism and molecular transport as the biological processes altered after high glucose treatment, followed by inflammation and apoptosis. Aspalathin was able to modulate key regulators associated with lipid metabolism (Adipoq, Apob, CD36, Cpt1, Pparγ, Srebf1/2, Scd1 and Vldlr), insulin resistance (Igf1, Akt1, Pde3 and Map2k1), inflammation (Il3, Il6, Jak2, Lepr, Socs3, and Tnf13) and apoptosis (Bcl2 and Chuk). Collectively, our results suggest that aspalathin could reverse metabolic abnormalities by activating Adipoq while modulating the expression of Pparγ and Srebf1/2, decreasing inflammation via Il6/Jak2 pathway, which together with an observed increased expression of Bcl2 prevents myocardium apoptosis.

Indexed as

AnimalsApoptosisCardiotonic AgentsCell LineChalconesCytokinesDiabetes Mellitus, ExperimentalFatty AcidsGene Expression ProfilingGene Expression RegulationInsulin ResistanceLeptinLipid MetabolismLipidsMaleMiceaspalathinCardiotonic AgentsChalconesCytokinesFatty AcidsLeptinLipidsPlant Extractsaspalathincardiomyopathydiabetes mellitushyperglycemialipotoxicitypolyphenols

Identifiers

PMID28146135
PMCPMC6155936
OpenAlexW2584060009

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.