Abstract
BackgroundTrace elements function as essential cofactors that are involved in various biochemical processes in mammals. Autophagy is vital for nutrient supplement, which is an important Zeitegber for the circadian homeostasis in heart. Here, we considered the possibility that autophagy, as well as the cardiomyocyte clock and glycolysis are interlinked. Detrimental effects were observed when cardiac system is exposed to bromine containing drugs. This study investigated the effects and mechanisms of bromide on the circadian clock and glycolytic metabolism of H9C2 cardiomyocytes.ResultsIn the present study, bromide does not affect cell viability and apoptosis of H9C2 cardiomyocytes. Bromide dampens the clock and glycolytic (Hk2 and Pkm2) gene expression rhythmicity in a dose-dependent manner. Additionally, bromide inhibits autophagic process in H9C2 cardiomyocytes. In contrast, rapamycin (an autophagy inducer) dramatically restores the inhibitory effect of NaBr on the mRNA expression levels of clock genes (Bmal1, Cry1 and Rorα) and glycolytic genes (Hk2 and Pkm2).ConclusionsOur results reveal that bromide represses the clock and glycolytic gene expression patterns, partially through inhibition of autophagy.
Highlights
Trace elements function as essential cofactors that are involved in various biochemical processes in mammals
Bromide does not affect survival and apoptosis of H9C2 cardiomyocytes To investigate the effects of bromide on the cardiomyocytes, we firstly assessed the toxicity of Sodium bromide (NaBr)
Similar tendency was observed in isolated rat neonatal primary cardiomyocytes when treated with the same doses of NaBr (Fig. S1)
Summary
Trace elements function as essential cofactors that are involved in various biochemical processes in mammals. The concentrations of bromide are negatively correlated with the lipids including TG, TC, and HDL-C in the human and rat plasma [6]. Coincidence with these findings, bromide exhibits beneficial effects on the FFA-induced lipid dysregulation in mouse hepatocytes, increasing its possibility in the treatment of metabolic disorders such as hepatic steatosis [7].
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