Preprint Article Version 1 This version not peer reviewed

Transcription Profile Unveils the Cardioprotective Effect of Aspalathin against Lipid Toxicity

Version 1 : Received: 17 November 2016 / Approved: 17 November 2016 / Online: 17 November 2016 (11:19:37 CET)

A peer-reviewed article of this Preprint also exists.

Johnson, R.; Dludla, P.V.; Muller, C.J.F.; Huisamen, B.; Essop, M.F.; Louw, J. The Transcription Profile Unveils the Cardioprotective Effect of Aspalathin against Lipid Toxicity in an In Vitro H9c2 Model. Molecules 2017, 22, 219. Johnson, R.; Dludla, P.V.; Muller, C.J.F.; Huisamen, B.; Essop, M.F.; Louw, J. The Transcription Profile Unveils the Cardioprotective Effect of Aspalathin against Lipid Toxicity in an In Vitro H9c2 Model. Molecules 2017, 22, 219.

Journal reference: Molecules 2017, 22, 219
DOI: 10.3390/molecules22020219

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

Readers' Comments and Ratings (0)

Leave a public comment
Send a private comment to the author(s)
Rate this article
Views 0
Downloads 0
Comments 0
Metrics 0
Leave a public comment

×
Alerts
Notify me about updates to this article or when a peer-reviewed version is published.