Phenylpyruvic Acid-2-O-β-D-Glucoside Attenuates High Glucose-Induced Apoptosis in H9c2 Cardiomyocytes

Dludla, Phiwayinkosi V.; Muller, Christo J. F.; Joubert, Elizabeth; Louw, Johan; Gabuza, Kwazi B.; Huisamen, Barbara; Essop, M. Faadiel; Johnson, Rabia

doi:10.1055/s-0042-110856

Cited by 20 publications

(30 citation statements)

References 34 publications

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“…However, aspalathin treatment suppressed this effect, which was associated with reduced FFA uptake and oxidation ( Figure 1 and Table 2 ). This result was in agreement with our previous findings [ 10 , 21 ].…”

Section: Resultssupporting

confidence: 94%

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

et al. 2017

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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.

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Section: Resultssupporting

confidence: 94%

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

et al. 2017

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“…Accumulative data is increasingly reporting on the cardioprotective properties of various pharmacological products in the treatment and prevention of DM and its complications [35–38]. Recently, our group has explored phytochemical compounds for their protective effect against DCM in cultured cardiomyocytes and diabetic mice [37–40].…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective potential of N-acetyl cysteine against hyperglycaemia-induced oxidative damage: a protocol for a systematic review

et al. 2017

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BackgroundHyperglycaemia-induced oxidative damage is a well-established factor implicated in the development of diabetic cardiomyopathy (DCM) in diabetic individuals. Some of the well-known characteristics of DCM include increased myocardial left ventricular wall thickness and remodelling that result in reduced cardiac efficiency. To prevent this, an increasing number of pharmacological compounds such as N-acetyl cysteine (NAC) are explored for their antioxidant properties. A few studies have shown that NAC can ameliorate hyperglycaemia-induced oxidative damage within the heart. Hence, the objective of this review is to synthesise the available evidence pertaining to the cardioprotective role of NAC against hyperglycaemia-induced oxidative damage and thus prevent DCM.MethodsThis systematic review protocol will be reported in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols (PRISMA-P) 2015 statement. We will perform a comprehensive search on major databases such as EMBASE, Cochrane Library, PubMed and Google scholar for original research articles published from January 1960 to March 2017. We will only report on literature that is available in English. Two authors will independently screen for eligible studies using pre-defined criteria, and data extraction will be done in duplicate. All discrepancies will be resolved by consensus or consultation of a third reviewer. The quality of studies will be checked using Cochrane Risk of Bias Assessment Tool and The Joanna Briggs Institute (JBI) Critical Appraisal tools for non-randomised experimental studies. Heterogeneity across studies will be assessed using the Cochrane Q statistic and the inconsistency index (I 2). We will use the random effects model to calculate a pooled estimate.DiscussionAlthough several studies have shown that NAC can ameliorate hyperglycaemia-induced oxidative damage within the heart, this systematic review will be the first pre-registered synthesis of data to identify the cardioprotective potential of NAC against hyperglycaemia-induced oxidative damage. This result will help guide future research evaluating the cardioprotective role of NAC against DCM and better identify possible mechanisms of action for NAC to prevent oxidative damage with a diabetic heart.Systemic review registrationPROSPERO CRD42017055851.Electronic supplementary materialThe online version of this article (doi:10.1186/s13643-017-0493-8) contains supplementary material, which is available to authorized users.

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“…Cumulative evidence suggests that either the individual rooibos components 9,23,24 or the crude rooibos extract/ tea confers cardioprotection against heart disease in diabetes 10 and heart attacks 25 . In one recent study, rooibos conferred cardioprotection in rats that were on antiretroviral therapy and displayed myocardial ischaemic damage.…”

Section: Introductionmentioning

confidence: 99%

Cardioprotection conferred by rooibos (Aspalathus linearis): A mini review to highlight a potential mechanism of action

Maarman¹

2019

S. Afr. J. Sci.

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Cardioprotection conferred by rooibos is likely via an AMPK-GLUT-4 glucose oxidation pathway. •The mechanism of cardioprotection is important for future studies investigating how rooibos alters cardiac mitochondria. •The more information gathered about the underlying mechanisms of rooibos, the easier it will be to recommend rooibos as an official cardioprotective intervention in patients with heart disease. Overview of cardiac energy substrate utilisation in cardioprotectionCardiac energy substrate utilisation plays a key role in cardiomyopathies 28,29 and cardioprotection 30,31 . In diabetes 32,33 , high blood glucose (hyperglycaemia) as well as high glucose uptake without simultaneous glucose utilisation/oxidation, Volume 115| Number 7/8

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Phenylpyruvic Acid-2-O-β-D-Glucoside Attenuates High Glucose-Induced Apoptosis in H9c2 Cardiomyocytes

Cited by 20 publications

References 34 publications

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

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

Cardioprotective potential of N-acetyl cysteine against hyperglycaemia-induced oxidative damage: a protocol for a systematic review

Cardioprotection conferred by rooibos (Aspalathus linearis): A mini review to highlight a potential mechanism of action

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