Trace 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. In 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). Our results reveal that bromide represses the clock and glycolytic gene expression patterns, partially through inhibition of autophagy.

中文翻译：

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溴化物通过破坏大鼠H9C2心肌细胞的自噬而损害昼夜节律和糖酵解稳态。

微量元素作为参与哺乳动物各种生化过程的必需辅助因子。自噬对于营养补充至关重要，营养补充是心脏昼夜动态平衡的重要Zeitegber。在这里，我们考虑了自噬以及心肌细胞时钟和糖酵解相互联系的可能性。当心脏系统暴露于含溴药物时，观察到有害作用。这项研究调查了溴化物对H9C2心肌细胞的昼夜节律和糖酵解代谢的影响及其机制。在本研究中，溴化物不影响H9C2心肌细胞的活力和凋亡。溴化物以剂量依赖性方式抑制时钟和糖酵解（Hk2和Pkm2）基因表达的节律性。另外，溴化物抑制H9C2心肌细胞的自噬过程。相反，雷帕霉素（一种自噬诱导剂）可显着恢复NaBr对时钟基因（Bmal1，Cry1和Rorα）和糖酵解基因（Hk2和Pkm2）的mRNA表达水平的抑制作用。我们的结果表明，溴化物可部分抑制自噬，从而抑制时钟和糖酵解基因的表达方式。