Preprint Article Version 1 NOT YET PEER-REVIEWED

Transcription Profile Unveils the Cardioprotective Effect of Aspalathin against Lipid Toxicity

  1. Biomedical Research and Innovation Platform (BRIP), Medical Research Council (MRC), Tygerberg, South Africa
  2. Division of Medical Physiology, Faculty of Health Sciences, Stellenbosch University, Tygerberg, South Africa
  3. Cardio-Metabolic Research Group (CMRG), Department of Physiological Sciences, Stellenbosch University, Stellenbosch, South Africa
Version 1 : Received: 17 November 2016 / Approved: 17 November 2016 / Online: 17 November 2016 (11:19:37 CET)

How to cite: Johnson, R.; Dludla, P.; Muller, C.; Huisamen, B.; Essop, M.; Louw, J. Transcription Profile Unveils the Cardioprotective Effect of Aspalathin against Lipid Toxicity. Preprints 2016, 2016110094 (doi: 10.20944/preprints201611.0094.v1). Johnson, R.; Dludla, P.; Muller, C.; Huisamen, B.; Essop, M.; Louw, J. Transcription Profile Unveils the Cardioprotective Effect of Aspalathin against Lipid Toxicity. Preprints 2016, 2016110094 (doi: 10.20944/preprints201611.0094.v1).

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 cardiomyocytes model. Cardiomyocytes were exposed to high glucose (33 mM) for 48 hours 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. 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 propose 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.

Subject Areas

diabetes mellitus; hyperglycemia; cardiomyopathy; lipid toxicity; polyphenols; aspalathin

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