The transcription profile unveils the cardioprotective effect of aspalathin against lipid toxicity in an in Vitro H9c2 model

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dc.contributor.authorJohnson, Rabiaen_ZA
dc.contributor.authorDludla, Phiwayinkosi V.en_ZA
dc.contributor.authorMuller, Christo J. F.en_ZA
dc.contributor.authorHuisamen, Barbaraen_ZA
dc.contributor.authorEssop, M. Faadielen_ZA
dc.contributor.authorLouw, Johanen_ZA
dc.date.accessioned2018-01-24T14:25:45Z
dc.date.available2018-01-24T14:25:45Z
dc.date.issued2017
dc.descriptionCITATION: Johnson, R., et al. 2017. The transcription profile unveils the cardioprotective effect of aspalathin against lipid toxicity in an in Vitro H9c2 model. Molecules, 22(2):219, doi:10.3390/molecules22020219.
dc.descriptionThe original publication is available at http://www.mdpi.com
dc.description.abstractAspalathin, 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, PparĪ³, 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 PparĪ³ and Srebf1/2, decreasing inflammation via Il6/Jak2 pathway, which together with an observed increased expression of Bcl2 prevents myocardium apoptosis.en_ZA
dc.description.urihttp://www.mdpi.com/1420-3049/22/2/219
dc.description.versionPublisher's versionen_ZA
dc.format.extent17 pages : illustrationsen_ZA
dc.identifier.citationJohnson, R., et al. 2017. The transcription profile unveils the cardioprotective effect of aspalathin against lipid toxicity in an in Vitro H9c2 model. Molecules, 22(2):219, doi:10.3390/molecules22020219
dc.identifier.issn1420-3049 (online)
dc.identifier.otherdoi:10.3390/molecules22020219
dc.identifier.urihttp://hdl.handle.net/10019.1/103086
dc.language.isoen_ZAen_ZA
dc.publisherMDPIen_ZA
dc.rights.holderAuthors retain copyrighten_ZA
dc.subjectDiabetes mellitusen_ZA
dc.subjectHyperglycemiaen_ZA
dc.subjectCardiomyopathyen_ZA
dc.subjectAspalathinen_ZA
dc.titleThe transcription profile unveils the cardioprotective effect of aspalathin against lipid toxicity in an in Vitro H9c2 modelen_ZA
dc.typeArticleen_ZA
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