Boron is an essential trace element in cellular metabolism; however, the molecular mechanism of boron in the heart is unclear. In this study, we examined the effect of sodium tetraborate (as boron source) as a possible protective agent or competitive inhibitor of cardiac hypertrophy in an in vitro murine model.

We evaluated different previously reported sodium tetraborate concentrations and it was found that 13 μM improves viability without affecting the cellular structure.

We demonstrated that cardiomyocytes pretreated with sodium tetraborate prevents cellular damage induced by isoproterenol (cardioprotective effect) by increasing proliferation rate and inhibiting apoptosis. In addition, the reduction of the expression of the α1AR and β1AR adrenergic receptors as well as Erk1/2 was notable. Consequently, the expression of the early response genes c-myc, c-fos and c-jun was delayed. Also, the expression of GATA-4, NFAT, NKx2.5 and myogenin transcription factors involved in sarcomere synthesis declined. In contrast, cardiomyocytes, when treated simultaneously with sodium tetraborate and isoproterenol, did not increase their size (cytoplasmic gain), but an increase in apoptosis levels was observed; therefore, the proliferation rate was reduced. Although the mRNA levels of α1AR and β1AR as well as Erk1/2 and Akt1 were low at 24 h, their expression increased to 48 h. Notably, the mRNA of expression levels of c-myc, c-fos and c-jun were lower than those determined in the control, while the transcription factors GATA-4, MEF2c, Nkx2.5, NFAT and CDk9 were determined in most cells.

These results suggest that pretreatment with sodium tetraborate in cardiomyocytes inhibits the hypertrophic effect. However, sodium tetraborate attenuates isoproterenol induced hypertrophy damage in cardiomyocytes when these two compounds are added simultaneously.

硼是细胞代谢中必不可少的微量元素；然而，硼在心脏中的分子机制尚不清楚。在这项研究中，我们在体外小鼠模型中检查了四硼酸钠（作为硼源）作为心脏肥大的可能保护剂或竞争性抑制剂的作用。

我们评估了不同的先前报道的四硼酸钠浓度，发现 13 μM 提高了活力而不影响细胞结构。

我们证明用四硼酸钠预处理的心肌细胞通过增加增殖率和抑制细胞凋亡来防止异丙肾上腺素诱导的细胞损伤（心脏保护作用）。此外，α1AR 和 β1AR 肾上腺素能受体以及 Erk1/2 的表达降低是显着的。因此，早期反应基因c-myc、c-fos 和 c-jun 的表达被延迟了。此外，参与肌节合成的 GATA-4、NFAT、NKx2.5 和肌细胞生成素转录因子的表达下降。相比之下，当用四硼酸钠和异丙肾上腺素同时处理时，心肌细胞没有增加它们的大小（细胞质增加），但观察到细胞凋亡水平增加；因此，扩散率降低了。尽管 α1AR 和 β1AR 以及 Erk1/2 和 Akt1 的 mRNA 水平在 24 小时时较低，但它们的表达增加到 48 小时。值得注意的是，c-myc、c-fos 和 c-jun的 mRNA 表达水平低于对照中测定的水平，而在大多数细胞中测定了转录因子 GATA-4、MEF2c、Nkx2.5、NFAT 和 CDk9 .

这些结果表明在心肌细胞中用四硼酸钠预处理可抑制肥大效应。然而，当这两种化合物同时加入时，四硼酸钠可减轻异丙肾上腺素诱导的心肌细胞肥大损伤。