Abstract
Myocardial fibrosis is a major determinant of clinical outcomes in heart failure (HF) patients. It is characterized by the emergence of myofibroblasts and early activation of pro-fibrotic signaling pathways before adverse ventricular remodeling and progression of HF. Boron has been reported in recent years to augment the innate immune system and cell proliferation, which play an important role in the repair and regeneration of the injured tissue. Currently, the effect of boron on cardiac contractility and remodeling is unknown. In this study, we investigated, for the first time, the effect of boron supplementation on cardiac function, myocardial fibrosis, apoptosis and regeneration in a rat model myocardial infarction (MI)-induced HF. MI was induced in animals and borax, a sodium salt of boron, was administered for 7 days, p.o., 21 days post-injury at a dose level of 4 mg/kg body weight. Transthoracic echocardiographic analysis showed a significant improvement in systolic and diastolic functions with boron treatment compared to saline control. In addition, boron administration showed a marked reduction in myocardial fibrosis and apoptosis in the injured hearts, highlighting a protective effect of boron in the ischemic heart. Interestingly, we observed a tenfold increase of nuclei in thin myocardial sections stained positive for the cell cycle marker Ki67 in the MI boron-treated rats compared to saline, indicative of increased cardiomyocyte cell cycle activity in MI hearts, highlighting its potential role in regeneration post-injury. We similarly observed increased Ki67 and BrdU staining in cultured fresh neonatal rat ventricular cardiomyocytes. Collectively, the results show that boron positively impacted MI-induced HF and attenuated cardiac fibrosis and apoptosis, two prominent features of HF. Importantly, boron has the potential to induce cardiomyocyte cell cycle entry and potentially cardiac tissue regeneration after injury. Boron might be beneficial as a supplement in MI and may be a good candidate substance for anti-fibrosis approach.
Highlights
Myocardial fibrosis is a major determinant of clinical outcomes in heart failure (HF) patients
Left ventricular (LV) function and dimensions were measured at baseline (Supplement Table 1), at 21 days after myocardial infarction (MI) operation and 7 days post treatment (Table 1)
Several non-mammalian vertebrates preserve the capacity for a scar-free healing and regeneration, but in human and most mammals, survival depends on the ability to repair and regenerate the tissue post-injury
Summary
Myocardial fibrosis is a major determinant of clinical outcomes in heart failure (HF) patients. In view of the role of boron on macrophage polarization – an adaptive component of the innate immunity which plays an important and complex role throughout the acute inflammatory and regenerative response – and its effect on cell p roliferation[6,7], we hypothesized the potential beneficial effect of boron in cardiac tissue remodeling, cardiomyocyte cell cycle activity and regeneration post cardiac injury/MI This is the first study of its kind where a metalloid (boron), a Group 13 chemical element of the Periodic Table, found in close proximity of carbon, one of the six elements (H, C, N, O, P and S) that came together to form life on earth, is reported to improve the cardiac health postinjury. The study implicates boron as a supplement/drug to attenuate fibrosis and for potential regeneration of the cardiac tissue post-injury
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